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il 1β elisa kit  (ABclonal Biotechnology)
97
ABclonal Biotechnology il 1β elisa kit
Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Il 1β Elisa Kit, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+il+1%CE%B2/Mouse+IL-1+beta+ELISA+Kit/pmc13616302-24-0-4
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il 1β elisa kit - by Bioz Stars, 2026-10
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mouse il1β  (Elabscience Biotechnology)
97
Elabscience Biotechnology mouse il1β
Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Mouse Il1β, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse il 1β elisa kit elabscience  (Elabscience Biotechnology)
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Elabscience Biotechnology mouse il 1β elisa kit elabscience
Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Mouse Il 1β Elisa Kit Elabscience, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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duoset elisa l 1β  (R&D Systems)
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R&D Systems duoset elisa l 1β
Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Duoset Elisa L 1β, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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il 1β  (Elabscience Biotechnology)
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Elabscience Biotechnology il 1β
Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Il 1β, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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elisa kits  (Cusabio)
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Cusabio elisa kits
Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Elisa Kits, supplied by Cusabio, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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il 1β elisa dy401  (R&D Systems)
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Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by <t>ELISA</t> ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Il 1β Elisa Dy401, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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elisa kit  (Elabscience Biotechnology)
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Elabscience Biotechnology elisa kit
KF alleviated fibrosis and inflammatory cytokines in mice. (A,B) Masson staining was used to detect colonic fibrosis and collagen deposition (magnification: 200×, scale bars: 150 µm) (each group: n = 6). (C–E) <t>ELISA</t> assay for determining the levels of inflammatory cytokines (each group: n = 6). (F–I) The expression levels of tumor necrosis factor α (TNF-α), zonula occludens-1 (ZO-1) and alpha smooth muscle actin (α-SMA) in colon tissues were measured by western blot. Glyceraldehyde -3-phosphate dehydrogenase (GAPDH) was the internal parameter (each group: n = 6). (J) Transepithelial electrical resistance the Ussing chamber experiment (each group: n = 6). *** P < 0.001 vs. Con; ^ P < 0.05, ^^ P < 0.01, ^^^ P < 0.001 vs. Mod.
Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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interleukin 1β  (Elabscience Biotechnology)
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Elabscience Biotechnology interleukin 1β
KF alleviated fibrosis and inflammatory cytokines in mice. (A,B) Masson staining was used to detect colonic fibrosis and collagen deposition (magnification: 200×, scale bars: 150 µm) (each group: n = 6). (C–E) <t>ELISA</t> assay for determining the levels of inflammatory cytokines (each group: n = 6). (F–I) The expression levels of tumor necrosis factor α (TNF-α), zonula occludens-1 (ZO-1) and alpha smooth muscle actin (α-SMA) in colon tissues were measured by western blot. Glyceraldehyde -3-phosphate dehydrogenase (GAPDH) was the internal parameter (each group: n = 6). (J) Transepithelial electrical resistance the Ussing chamber experiment (each group: n = 6). *** P < 0.001 vs. Con; ^ P < 0.05, ^^ P < 0.01, ^^^ P < 0.001 vs. Mod.
Interleukin 1β, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by ELISA ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: AI‐Designed TREM1‐Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury

doi: 10.1002/advs.77972

Figure Lengend Snippet: Systemic TREM1 ablation attenuates neuroinflammation and neurological deficits after TBI. (a) Schematic timeline of the experimental design. WT and Trem1 −/− mice were subjected to CCI or sham surgery, followed by longitudinal behavioral and histological assessments. (b, c) Analysis of the neuroinflammatory profile in the perilesional cortex at 3 days post‐TBI. (b) Representative images of inflammatory cytokines in TBI lesions detected by the Proteome Profiler Array Mouse Cytokine Array Panel A in WT and Trem1 −/− mice at 3 days post‐TBI. (c) Quantification of inflammatory cytokines in TBI lesions of WT and Trem1 −/− mice at 3 days post‐TBI or sham treatment by ELISA ( n = 5 mice per group, two‐way ANOVA followed by Tukey's multiple‐comparison test). (d) Representative immunofluorescence images of macrophages (IBA1 + , green) and the reactivation marker CD86 (red) in the TBI cortex. Trem1 ablation significantly reduced reactive polarization (scale bar, 50 µm). (e) Evaluation of neuronal apoptosis. Representative co‐staining of TUNEL (green) and NeuN (red) (left) ( n = 3 mice per group, scale bar, 100 µm). Yellow arrows indicate apoptotic neurons. (f) Assessment of white matter integrity. Representative images of Myelin Basic Protein (MBP, green) and NeuN (red) (left) and quantification of MBP fluorescence intensity (right) (scale bar, 100 µm). (g) Representative immunofluorescence images of hippocampal neurons (NeuN, red) showing preserved cellular density in Trem1 −/− mice ( n = 3 mice per group; scale bar, 100 µm). (h) Brain water content analysis at 1day and 3 d post‐TBI, indicating alleviated cerebral edema in Trem1 −/− mice ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (i, j) Assessment of blood‐brain barrier (BBB) permeability. (i) Representative images of Evans Blue extravasation. (j) Quantification of dye leakage ( n = 6 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (k, l) Molecular validation of tissue preservation. (k) Representative Western blots of the neuronal marker beta3‐tubulin, synaptic marker Synaptophysin (Syn), and tight junction protein Occludin. l, Densitometric quantification normalized to GAPDH ( n = 3 independent experimental replicates; two‐way ANOVA followed by Tukey's multiple‐comparison test). (m–o) Assessment of sensorimotor function. m, Latency to fall in the accelerating Rotarod test ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (n) Performance in the fixed‐speed (30 rpm) Rotarod test ( n = 8 mice per group, one‐way ANOVA followed by Tukey's multiple‐comparison test). o, Modified Neurological Severity Score (mNSS) trajectory ( n = 8 mice per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). (p, q) Evaluation of anxiety‐like behavior and exploratory activity in the Open Field Test (OFT). (p) Representative locomotor tracking plots. (q) Quantification of the percentage of time spent in the center zone ( n = 8 per group; two‐way ANOVA followed by Tukey's multiple‐comparison test). Data are presented as mean ± SD. Each dot represents an individual mouse, except in l, where each dot represents an independent experimental replicate. Statistical tests are specified for each panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: IL‐1β ELISA kit , ABclonal , # RK00006.

Techniques: Analysis, Enzyme-linked Immunosorbent Assay, Comparison, Immunofluorescence, Marker, Staining, TUNEL Assay, Fluorescence, Permeability, Biomarker Discovery, Tissue, Preserving, Western Blot, Modification, Activity Assay

Generative AI‐driven design and mechanistic validation of a TREM1‐targeting LYTAC degrader. (a) Schematic of the RFdiffusion‐guided pipeline for de novo TREM1‐binding peptide design. Peptide backbones were generated around the Ig‐like domain of TREM1 and subsequently screened by AlphaFold3, ZDOCK, HDOCK, and Rosetta‐based energetic analysis to identify high‐ranking candidates. (b) Predicted structural models of Pep15, Pep17, and Pep457 in complex with TREM1, showing the predicted binding interfaces. (c) Temperature‐related intensity change (TRIC) assays showing concentration‐dependent target engagement of Pep15, Pep17, and Pep457 with TREM1. Left, schematic illustration of the TRIC assay principle; right, dose‐response curves of the indicated peptides ( n = 3 independent experiments). (d) ELISA‐based binding analysis of Pep15, Pep17, and Pep457 to immobilized TREM1. Top, schematic of the ELISA workflow; bottom, quantitative binding curves ( n = 3 independent experiments). (e) Surface plasmon resonance (SPR) analysis of Pep457 binding to TREM1. Top, schematic of the SPR assay; bottom, representative sensorgrams obtained at the indicated Pep457 concentrations. (f) Structural model of the bifunctional TREM1‐LYTAC, in which Pep457 engages TREM1 and the mannose‐6‐phosphate (M6P) moiety recruits the cation‐independent mannose‐6‐phosphate receptor (CI‐M6PR). (g) Representative confocal images showing partial colocalization of TREM1‐LYTAC with lysosomes following cellular uptake. TREM1‐LYTAC, green; lysosomes, red; nuclei, blue. Arrows indicate representative colocalized puncta. Scale bars as indicated. (h) ELISA quantification of cellular TREM1 protein following treatment with vehicle, scrambled‐LYTAC, TREM1‐LYTAC, or TREM1‐LYTAC in the presence of bafilomycin A1 (BafA1) or MG132 ( n = 5 independent experiments). (i) Representative flow‐cytometric histograms showing cell‐surface TREM1 expression after the indicated treatments. (j) Trem1 mRNA expression measured by qPCR after the indicated treatments ( n = 3 independent experiments; one‐way ANOVA followed by Tukey's multiple‐comparison test). (k) Requirement of both functional modules for TREM1 reduction. Cellular TREM1 protein levels were quantified after treatment with Pep457 plus M6P, Pep457 alone, M6P alone, TREM1‐LYTAC in the presence of CI‐M6PR blockade, or conjugated TREM1‐LYTAC ( n = 5 independent experiments; one‐way ANOVA followed by Tukey's multiple‐comparison test). (l) Plasma pharmacokinetic profile of free TREM1‐LYTAC after intravenous administration. Fluorescence intensity was fitted to a monoexponential decay model, yielding an apparent half‐life of 1.13 h ( n = 3 mice). (m) Proposed mechanism of TREM1‐LYTAC‐mediated degradation. TREM1‐LYTAC bridges cell‐surface TREM1 to CI‐M6PR, thereby promoting receptor internalization and lysosomal degradation. Data are mean ± SD. Each dot represents an independent experimental replicate or an individual animal. Statistical tests are specified for each quantitative panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: AI‐Designed TREM1‐Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury

doi: 10.1002/advs.77972

Figure Lengend Snippet: Generative AI‐driven design and mechanistic validation of a TREM1‐targeting LYTAC degrader. (a) Schematic of the RFdiffusion‐guided pipeline for de novo TREM1‐binding peptide design. Peptide backbones were generated around the Ig‐like domain of TREM1 and subsequently screened by AlphaFold3, ZDOCK, HDOCK, and Rosetta‐based energetic analysis to identify high‐ranking candidates. (b) Predicted structural models of Pep15, Pep17, and Pep457 in complex with TREM1, showing the predicted binding interfaces. (c) Temperature‐related intensity change (TRIC) assays showing concentration‐dependent target engagement of Pep15, Pep17, and Pep457 with TREM1. Left, schematic illustration of the TRIC assay principle; right, dose‐response curves of the indicated peptides ( n = 3 independent experiments). (d) ELISA‐based binding analysis of Pep15, Pep17, and Pep457 to immobilized TREM1. Top, schematic of the ELISA workflow; bottom, quantitative binding curves ( n = 3 independent experiments). (e) Surface plasmon resonance (SPR) analysis of Pep457 binding to TREM1. Top, schematic of the SPR assay; bottom, representative sensorgrams obtained at the indicated Pep457 concentrations. (f) Structural model of the bifunctional TREM1‐LYTAC, in which Pep457 engages TREM1 and the mannose‐6‐phosphate (M6P) moiety recruits the cation‐independent mannose‐6‐phosphate receptor (CI‐M6PR). (g) Representative confocal images showing partial colocalization of TREM1‐LYTAC with lysosomes following cellular uptake. TREM1‐LYTAC, green; lysosomes, red; nuclei, blue. Arrows indicate representative colocalized puncta. Scale bars as indicated. (h) ELISA quantification of cellular TREM1 protein following treatment with vehicle, scrambled‐LYTAC, TREM1‐LYTAC, or TREM1‐LYTAC in the presence of bafilomycin A1 (BafA1) or MG132 ( n = 5 independent experiments). (i) Representative flow‐cytometric histograms showing cell‐surface TREM1 expression after the indicated treatments. (j) Trem1 mRNA expression measured by qPCR after the indicated treatments ( n = 3 independent experiments; one‐way ANOVA followed by Tukey's multiple‐comparison test). (k) Requirement of both functional modules for TREM1 reduction. Cellular TREM1 protein levels were quantified after treatment with Pep457 plus M6P, Pep457 alone, M6P alone, TREM1‐LYTAC in the presence of CI‐M6PR blockade, or conjugated TREM1‐LYTAC ( n = 5 independent experiments; one‐way ANOVA followed by Tukey's multiple‐comparison test). (l) Plasma pharmacokinetic profile of free TREM1‐LYTAC after intravenous administration. Fluorescence intensity was fitted to a monoexponential decay model, yielding an apparent half‐life of 1.13 h ( n = 3 mice). (m) Proposed mechanism of TREM1‐LYTAC‐mediated degradation. TREM1‐LYTAC bridges cell‐surface TREM1 to CI‐M6PR, thereby promoting receptor internalization and lysosomal degradation. Data are mean ± SD. Each dot represents an independent experimental replicate or an individual animal. Statistical tests are specified for each quantitative panel above. Exact p values are provided in the Source Data. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: IL‐1β ELISA kit , ABclonal , # RK00006.

Techniques: Biomarker Discovery, Binding Assay, Generated, Analysis, Concentration Assay, Drug discovery, Enzyme-linked Immunosorbent Assay, SPR Assay, Confocal, Expressing, Comparison, Functional Assay, Clinical Proteomics, Fluorescence

Engineering and validation of a BBB‐targeted, pH‐responsive nanodevice for spatiotemporal delivery of TREM1‐LYTAC. (a) Schematic illustration of APTL‐NP fabrication. TREM1‐LYTAC was conjugated to a generation‐4 PAMAM dendrimer through a terephthalaldehyde‐derived acid‐labile linker, followed by surface functionalization with Angiopep‐2 and PS‐PEG‐NHS to enable LRP1‐directed BBB targeting and improve systemic stability. (b) Representative transmission electron microscopy images of PAMAM‐based precursor particles and APTL‐NP (Scale bars, 1 µm). (c) Dynamic light scattering profiles showing the apparent hydrodynamic size distributions of G4 PAMAM and APTL‐NP under the indicated measurement conditions. (d) Time‐dependent changes in hydrodynamic diameter and polydispersity index of APTL‐NP incubated in PBS at pH 7.4 and 37°C. (e) pH‐dependent zeta‐potential profile of APTL‐NP. (f) Nanoparticle tracking analysis showing pH‐dependent particle size and concentration distributions after incubation at pH 7.5, 7.0, or 6.5. (g) pH‐responsive release of TREM1‐binding‐competent TREM1‐LYTAC from APTL‐NP. Released free TREM1‐LYTAC was separated by ultrafiltration and quantified using a TREM1‐binding ELISA with free TREM1‐LYTAC standards ( n = 3 independent experiments). (h) Representative EdU staining images of BMECs, HT22 cells, and NHAs treated with vehicle or APTL‐NP. (i) Quantification of EdU‐positive cells in the indicated cell types( n = 6 independent experiments, two‐way ANOVA followed by Tukey's multiple‐comparison test). (j) Representative flow‐cytometric plots for apoptosis analysis in BMECs, HT22 cells, and NHAs after treatment with vehicle or APTL‐NP. (k) Quantification of apoptotic cells in the indicated cell types( n = 6 independent experiments, two‐way ANOVA followed by Tukey's multiple‐comparison test). (l) Cell viability after 24 h or 48 h exposure to the indicated concentrations of APTL‐NP ( n = 3 independent experiments, two‐way ANOVA followed by Tukey's multiple‐comparison test). (m) Plasma pharmacokinetic profile of APTL‐NP after intravenous administration. The fluorescence signal was fitted to a monoexponential decay model, yielding an apparent half‐life of 8.38 h ( n = 3 mice). (n) Representative photographs and quantification of hemolysis induced by the indicated concentrations of APTL‐NP ( n = 3 independent experiments, one‐way ANOVA followed by Tukey's multiple‐comparison test). (o, p) Plasma C3a and C5a concentrations at the indicated time points after administration of vehicle or APTL‐NP ( n = 6 mice per group, Two‐way ANOVA followed by Tukey's multiple‐comparison test). (q) Representative H&E‐stained sections of the spleen, heart, lung, liver, and kidney from vehicle‐ and APTL‐NP‐treated mice (Scale bar, 100 µm). Data are presented as mean ± SD where applicable. For in vitro assays, n denotes independent experimental replicates; for in vivo analyses, n denotes individual mice. Statistical tests are specified for each quantitative panel above. Exact p values are provided in the Source Data. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: AI‐Designed TREM1‐Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury

doi: 10.1002/advs.77972

Figure Lengend Snippet: Engineering and validation of a BBB‐targeted, pH‐responsive nanodevice for spatiotemporal delivery of TREM1‐LYTAC. (a) Schematic illustration of APTL‐NP fabrication. TREM1‐LYTAC was conjugated to a generation‐4 PAMAM dendrimer through a terephthalaldehyde‐derived acid‐labile linker, followed by surface functionalization with Angiopep‐2 and PS‐PEG‐NHS to enable LRP1‐directed BBB targeting and improve systemic stability. (b) Representative transmission electron microscopy images of PAMAM‐based precursor particles and APTL‐NP (Scale bars, 1 µm). (c) Dynamic light scattering profiles showing the apparent hydrodynamic size distributions of G4 PAMAM and APTL‐NP under the indicated measurement conditions. (d) Time‐dependent changes in hydrodynamic diameter and polydispersity index of APTL‐NP incubated in PBS at pH 7.4 and 37°C. (e) pH‐dependent zeta‐potential profile of APTL‐NP. (f) Nanoparticle tracking analysis showing pH‐dependent particle size and concentration distributions after incubation at pH 7.5, 7.0, or 6.5. (g) pH‐responsive release of TREM1‐binding‐competent TREM1‐LYTAC from APTL‐NP. Released free TREM1‐LYTAC was separated by ultrafiltration and quantified using a TREM1‐binding ELISA with free TREM1‐LYTAC standards ( n = 3 independent experiments). (h) Representative EdU staining images of BMECs, HT22 cells, and NHAs treated with vehicle or APTL‐NP. (i) Quantification of EdU‐positive cells in the indicated cell types( n = 6 independent experiments, two‐way ANOVA followed by Tukey's multiple‐comparison test). (j) Representative flow‐cytometric plots for apoptosis analysis in BMECs, HT22 cells, and NHAs after treatment with vehicle or APTL‐NP. (k) Quantification of apoptotic cells in the indicated cell types( n = 6 independent experiments, two‐way ANOVA followed by Tukey's multiple‐comparison test). (l) Cell viability after 24 h or 48 h exposure to the indicated concentrations of APTL‐NP ( n = 3 independent experiments, two‐way ANOVA followed by Tukey's multiple‐comparison test). (m) Plasma pharmacokinetic profile of APTL‐NP after intravenous administration. The fluorescence signal was fitted to a monoexponential decay model, yielding an apparent half‐life of 8.38 h ( n = 3 mice). (n) Representative photographs and quantification of hemolysis induced by the indicated concentrations of APTL‐NP ( n = 3 independent experiments, one‐way ANOVA followed by Tukey's multiple‐comparison test). (o, p) Plasma C3a and C5a concentrations at the indicated time points after administration of vehicle or APTL‐NP ( n = 6 mice per group, Two‐way ANOVA followed by Tukey's multiple‐comparison test). (q) Representative H&E‐stained sections of the spleen, heart, lung, liver, and kidney from vehicle‐ and APTL‐NP‐treated mice (Scale bar, 100 µm). Data are presented as mean ± SD where applicable. For in vitro assays, n denotes independent experimental replicates; for in vivo analyses, n denotes individual mice. Statistical tests are specified for each quantitative panel above. Exact p values are provided in the Source Data. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: IL‐1β ELISA kit , ABclonal , # RK00006.

Techniques: Biomarker Discovery, Derivative Assay, Stability, Transmission Assay, Electron Microscopy, Dynamic Light Scattering Assay, Incubation, Zeta Potential Analyzer, Analysis, Concentration Assay, Binding Assay, Enzyme-linked Immunosorbent Assay, Staining, Comparison, Clinical Proteomics, Fluorescence, In Vitro, In Vivo

Key resources table.

Journal: Advanced Science

Article Title: AI‐Designed TREM1‐Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury

doi: 10.1002/advs.77972

Figure Lengend Snippet: Key resources table.

Article Snippet: IL‐1β ELISA kit , ABclonal , # RK00006.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Software

KF alleviated fibrosis and inflammatory cytokines in mice. (A,B) Masson staining was used to detect colonic fibrosis and collagen deposition (magnification: 200×, scale bars: 150 µm) (each group: n = 6). (C–E) ELISA assay for determining the levels of inflammatory cytokines (each group: n = 6). (F–I) The expression levels of tumor necrosis factor α (TNF-α), zonula occludens-1 (ZO-1) and alpha smooth muscle actin (α-SMA) in colon tissues were measured by western blot. Glyceraldehyde -3-phosphate dehydrogenase (GAPDH) was the internal parameter (each group: n = 6). (J) Transepithelial electrical resistance the Ussing chamber experiment (each group: n = 6). *** P < 0.001 vs. Con; ^ P < 0.05, ^^ P < 0.01, ^^^ P < 0.001 vs. Mod.

Journal: Frontiers in Pharmacology

Article Title: Kaempferol in inflammatory bowel disease: regulating intestinal epithelial-fibroblast crosstalk

doi: 10.3389/fphar.2026.1799034

Figure Lengend Snippet: KF alleviated fibrosis and inflammatory cytokines in mice. (A,B) Masson staining was used to detect colonic fibrosis and collagen deposition (magnification: 200×, scale bars: 150 µm) (each group: n = 6). (C–E) ELISA assay for determining the levels of inflammatory cytokines (each group: n = 6). (F–I) The expression levels of tumor necrosis factor α (TNF-α), zonula occludens-1 (ZO-1) and alpha smooth muscle actin (α-SMA) in colon tissues were measured by western blot. Glyceraldehyde -3-phosphate dehydrogenase (GAPDH) was the internal parameter (each group: n = 6). (J) Transepithelial electrical resistance the Ussing chamber experiment (each group: n = 6). *** P < 0.001 vs. Con; ^ P < 0.05, ^^ P < 0.01, ^^^ P < 0.001 vs. Mod.

Article Snippet: According to the instructions of the ELISA kit (E-EL-M0037, E-EL-M0044, E-EL-M3063, E-EL-H0149, E-EL-H6156, E-EL-H0109, E-EL-0162, E-EL-H2172, E-EL-H0084, Elabscience, China), samples were added sequentially, followed by the incubation with biotinylated antibody working solution and plate washing.

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

KF regulated HT29 cell inflammation and oxidative stress induced by TNF-α intervention. (A) Methylthiazolyldiphenyl-tetrazolium bromide (MTT) was employed to determine the cytotoxicity of KF against HT29 cells. (B–D) The protein expression levels of ZO-1 and HMOX1 in each group of cells were assessed by western blot. GAPDH was the internal parameter. (E,F) The level of transforming growth factor-β1 (TGF-β1) and HO-1 in the cell culture medium was detected by enzyme-linked immunosorbent assay (ELISA). (G,H) Western blot was used to examine the NRF2 nuclear translocation. GAPDH, LaminB1 was the internal parameter. (I) Flow cytometry-based detection of intracellular reactive oxygen species (ROS) generation. (J) The level of SOD was detected by commercially available kits. (K–M) ELISA assay for determining the levels of inflammatory cytokine (IL-1β, IL-6 and TNF-α). Each experiment was repeated 3 times. ** P < 0.01, *** P < 0.001 vs. Con; + P < 0.05, +++ P < 0.001 vs. TNF-α; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. KF.

Journal: Frontiers in Pharmacology

Article Title: Kaempferol in inflammatory bowel disease: regulating intestinal epithelial-fibroblast crosstalk

doi: 10.3389/fphar.2026.1799034

Figure Lengend Snippet: KF regulated HT29 cell inflammation and oxidative stress induced by TNF-α intervention. (A) Methylthiazolyldiphenyl-tetrazolium bromide (MTT) was employed to determine the cytotoxicity of KF against HT29 cells. (B–D) The protein expression levels of ZO-1 and HMOX1 in each group of cells were assessed by western blot. GAPDH was the internal parameter. (E,F) The level of transforming growth factor-β1 (TGF-β1) and HO-1 in the cell culture medium was detected by enzyme-linked immunosorbent assay (ELISA). (G,H) Western blot was used to examine the NRF2 nuclear translocation. GAPDH, LaminB1 was the internal parameter. (I) Flow cytometry-based detection of intracellular reactive oxygen species (ROS) generation. (J) The level of SOD was detected by commercially available kits. (K–M) ELISA assay for determining the levels of inflammatory cytokine (IL-1β, IL-6 and TNF-α). Each experiment was repeated 3 times. ** P < 0.01, *** P < 0.001 vs. Con; + P < 0.05, +++ P < 0.001 vs. TNF-α; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. KF.

Article Snippet: According to the instructions of the ELISA kit (E-EL-M0037, E-EL-M0044, E-EL-M3063, E-EL-H0149, E-EL-H6156, E-EL-H0109, E-EL-0162, E-EL-H2172, E-EL-H0084, Elabscience, China), samples were added sequentially, followed by the incubation with biotinylated antibody working solution and plate washing.

Techniques: Expressing, Western Blot, Cell Culture, Enzyme-linked Immunosorbent Assay, Translocation Assay, Flow Cytometry

HO-1 inhibitors reverse the effects of KF, and KF can also influence HT29 cells in a co-culture system. (A) The viability of CCD-18Co cells was examined by CCK-8. (B–E) Western blot was used to quantify the levels of activation marker proteins in CCD-18Co cells, including MMP2/9 and α-SMA. GAPDH was the internal parameter. (F) The viability of HT-29 cells was detected by CCK-8. (G–I) ELISA assay for determining the levels of inflammatory cytokine (IL-1β, IL-6 and TNF-α). (J) ELISA was used to measure the level of hepatocyte growth factor (HGF) in the culture medium. (K,L) The protein level of ZO-1 in HT29 was tested by western blot. GAPDH was the internal parameter. Each experiment was repeated 3 times. + P < 0.05, ++ P < 0.01, +++ P < 0.001 vs. TNF-α; Ω P <0.05 vs. TNF-α+KF; * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Con; # P < 0.05, ### P < 0.001 vs. KF.

Journal: Frontiers in Pharmacology

Article Title: Kaempferol in inflammatory bowel disease: regulating intestinal epithelial-fibroblast crosstalk

doi: 10.3389/fphar.2026.1799034

Figure Lengend Snippet: HO-1 inhibitors reverse the effects of KF, and KF can also influence HT29 cells in a co-culture system. (A) The viability of CCD-18Co cells was examined by CCK-8. (B–E) Western blot was used to quantify the levels of activation marker proteins in CCD-18Co cells, including MMP2/9 and α-SMA. GAPDH was the internal parameter. (F) The viability of HT-29 cells was detected by CCK-8. (G–I) ELISA assay for determining the levels of inflammatory cytokine (IL-1β, IL-6 and TNF-α). (J) ELISA was used to measure the level of hepatocyte growth factor (HGF) in the culture medium. (K,L) The protein level of ZO-1 in HT29 was tested by western blot. GAPDH was the internal parameter. Each experiment was repeated 3 times. + P < 0.05, ++ P < 0.01, +++ P < 0.001 vs. TNF-α; Ω P <0.05 vs. TNF-α+KF; * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Con; # P < 0.05, ### P < 0.001 vs. KF.

Article Snippet: According to the instructions of the ELISA kit (E-EL-M0037, E-EL-M0044, E-EL-M3063, E-EL-H0149, E-EL-H6156, E-EL-H0109, E-EL-0162, E-EL-H2172, E-EL-H0084, Elabscience, China), samples were added sequentially, followed by the incubation with biotinylated antibody working solution and plate washing.

Techniques: Co-culture Assay, CCK-8 Assay, Western Blot, Activation Assay, Marker, Enzyme-linked Immunosorbent Assay