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BacGuard promotes colon tissue repairment. a) Scheme of microbiota-dependent epithelial repair mechanism orchestrated by BacGuard. b) Short-chain fatty acid (SCFA) profile alterations. n = 6. c) BacGuard-induced probiotic proliferation and d) quantitative results. n = 3. e) Immunofluorescence analysis of ILC3 (ROR γt + CD3 − cells) in colon tissue. f) Flow cytometric analysis of lamina propria lymphocytes (ROR γt + ). n = 3. g) Concentration <t>of</t> <t>IL-22</t> in MNK-3 cells. n = 3. h) Representative PAS-staining (upper panel) and MUC-2 immunohistochemistry (lower panel) images of colon tissues. n = 5. ns, not significant; ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001.
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Scatter plots of the association <t>between</t> <t>TNF-α</t> production and the IC 50 values (LDA and LMA) Scatter plots showing the association <t>between</t> <t>TNF-α</t> production percentage (expressed relative to the control) and the IC 50 values obtained in (left) the Larval Development Assay (LDA) and (right) the Larval Migration Assay (LMA) for six terpene compounds (anethole, cinnamaldehyde, menthol, carvacrol, eugenol and thymol). Each point represents the mean IC 50 and TNFα production for a given compound, and horizontal/vertical bars indicate the corresponding confidence intervals. Lower IC 50 values reflect higher antiparasitic potency.
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circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of <t>IL-10,</t> TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.
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Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and <t>IL-10,</t> and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).
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HFD leads to downregulation of the expression of adipose Cfd and hepatic C3 and Cfb (A and B) C3-tdTomato reporter mice were placed on LFD or HFD, and expression of inflammatory markers and complement genes were assessed by qPCR in (A) subcutaneous inguinal adipose tissue and (B) visceral epididymal adipose tissue. (C) Western blot for FD in serum from female LFD and HFD mice after 25 weeks of diet. (D) Western blot for FD in serum from male mice after 15 weeks of diet. (E) Left: representative western blot from sequential serum samples from 2 male mice on HFD. Right: densitometry for serum FD signal in western blots of 6 male mice over time. (F–H) Serum FD levels, measured by <t>ELISA,</t> plotted against individual mouse body weight (F), fasting insulin (G), and fasting blood glucose levels (H). (I) Expression of main alternative pathway components in livers of LFD and HFD mice. (J) Protein levels of C3 in liver homogenates from lean control or ob/ob mice on the C57Bl/6 background. WAT, white adipose tissue. In (A)–(C), there were 4 mice per group, except for HFD visceral fat pad, which had 3 samples. In (F)–(H), measurements are from a total of 42 individual mouse samples. For (I) and (J), there were 4–5 mice per group. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA. See also .
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HFD leads to downregulation of the expression of adipose Cfd and hepatic C3 and Cfb (A and B) C3-tdTomato reporter mice were placed on LFD or HFD, and expression of inflammatory markers and complement genes were assessed by qPCR in (A) subcutaneous inguinal adipose tissue and (B) visceral epididymal adipose tissue. (C) Western blot for FD in serum from female LFD and HFD mice after 25 weeks of diet. (D) Western blot for FD in serum from male mice after 15 weeks of diet. (E) Left: representative western blot from sequential serum samples from 2 male mice on HFD. Right: densitometry for serum FD signal in western blots of 6 male mice over time. (F–H) Serum FD levels, measured by <t>ELISA,</t> plotted against individual mouse body weight (F), fasting insulin (G), and fasting blood glucose levels (H). (I) Expression of main alternative pathway components in livers of LFD and HFD mice. (J) Protein levels of C3 in liver homogenates from lean control or ob/ob mice on the C57Bl/6 background. WAT, white adipose tissue. In (A)–(C), there were 4 mice per group, except for HFD visceral fat pad, which had 3 samples. In (F)–(H), measurements are from a total of 42 individual mouse samples. For (I) and (J), there were 4–5 mice per group. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA. See also .
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HFD leads to downregulation of the expression of adipose Cfd and hepatic C3 and Cfb (A and B) C3-tdTomato reporter mice were placed on LFD or HFD, and expression of inflammatory markers and complement genes were assessed by qPCR in (A) subcutaneous inguinal adipose tissue and (B) visceral epididymal adipose tissue. (C) Western blot for FD in serum from female LFD and HFD mice after 25 weeks of diet. (D) Western blot for FD in serum from male mice after 15 weeks of diet. (E) Left: representative western blot from sequential serum samples from 2 male mice on HFD. Right: densitometry for serum FD signal in western blots of 6 male mice over time. (F–H) Serum FD levels, measured by <t>ELISA,</t> plotted against individual mouse body weight (F), fasting insulin (G), and fasting blood glucose levels (H). (I) Expression of main alternative pathway components in livers of LFD and HFD mice. (J) Protein levels of C3 in liver homogenates from lean control or ob/ob mice on the C57Bl/6 background. WAT, white adipose tissue. In (A)–(C), there were 4 mice per group, except for HFD visceral fat pad, which had 3 samples. In (F)–(H), measurements are from a total of 42 individual mouse samples. For (I) and (J), there were 4–5 mice per group. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA. See also .
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Image Search Results


BacGuard promotes colon tissue repairment. a) Scheme of microbiota-dependent epithelial repair mechanism orchestrated by BacGuard. b) Short-chain fatty acid (SCFA) profile alterations. n = 6. c) BacGuard-induced probiotic proliferation and d) quantitative results. n = 3. e) Immunofluorescence analysis of ILC3 (ROR γt + CD3 − cells) in colon tissue. f) Flow cytometric analysis of lamina propria lymphocytes (ROR γt + ). n = 3. g) Concentration of IL-22 in MNK-3 cells. n = 3. h) Representative PAS-staining (upper panel) and MUC-2 immunohistochemistry (lower panel) images of colon tissues. n = 5. ns, not significant; ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001.

Journal: Bioactive Materials

Article Title: Dynamic feedback BacGuard anchors microbial metabolism to host symbiosis in real-time ulcerative colitis therapy

doi: 10.1016/j.bioactmat.2026.05.060

Figure Lengend Snippet: BacGuard promotes colon tissue repairment. a) Scheme of microbiota-dependent epithelial repair mechanism orchestrated by BacGuard. b) Short-chain fatty acid (SCFA) profile alterations. n = 6. c) BacGuard-induced probiotic proliferation and d) quantitative results. n = 3. e) Immunofluorescence analysis of ILC3 (ROR γt + CD3 − cells) in colon tissue. f) Flow cytometric analysis of lamina propria lymphocytes (ROR γt + ). n = 3. g) Concentration of IL-22 in MNK-3 cells. n = 3. h) Representative PAS-staining (upper panel) and MUC-2 immunohistochemistry (lower panel) images of colon tissues. n = 5. ns, not significant; ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001.

Article Snippet: For the detection of IL-22 and LPS concentrations, the Mouse IL-22 Precoated ELISA Kit (DAKEWE, China) and Mouse LPS ELISA Kit (JONLNBIO, China) were employed correspondingly.

Techniques: Immunofluorescence, Concentration Assay, Staining, Immunohistochemistry

Scatter plots of the association between TNF-α production and the IC 50 values (LDA and LMA) Scatter plots showing the association between TNF-α production percentage (expressed relative to the control) and the IC 50 values obtained in (left) the Larval Development Assay (LDA) and (right) the Larval Migration Assay (LMA) for six terpene compounds (anethole, cinnamaldehyde, menthol, carvacrol, eugenol and thymol). Each point represents the mean IC 50 and TNFα production for a given compound, and horizontal/vertical bars indicate the corresponding confidence intervals. Lower IC 50 values reflect higher antiparasitic potency.

Journal: International Journal for Parasitology: Drugs and Drug Resistance

Article Title: Terpenic compounds possess anthelmintic and immunomodulatory properties with potential for controlling equine cyathostomin infections

doi: 10.1016/j.ijpddr.2026.100642

Figure Lengend Snippet: Scatter plots of the association between TNF-α production and the IC 50 values (LDA and LMA) Scatter plots showing the association between TNF-α production percentage (expressed relative to the control) and the IC 50 values obtained in (left) the Larval Development Assay (LDA) and (right) the Larval Migration Assay (LMA) for six terpene compounds (anethole, cinnamaldehyde, menthol, carvacrol, eugenol and thymol). Each point represents the mean IC 50 and TNFα production for a given compound, and horizontal/vertical bars indicate the corresponding confidence intervals. Lower IC 50 values reflect higher antiparasitic potency.

Article Snippet: The cells were then incubated at +37 °C (5% CO 2 ) for 24 h. After incubation, the concentration of TNF-α in the medium for each condition was quantified by ELISA using mouse TNF-α paired antibodies (R and D Systems DY410).

Techniques: Control, Migration

Anti-inflammatory activity of carvacrol and cinnamaldehyde on equine PBMC Boxplots showing TNF-α concentrations (ng/mL) measured in equine peripheral blood mononuclear cells (PBMCs) exposed to DMSO (0.05%), LPS (125 ng/mL), the combination of DMSO and LPS, carvacrol (5 μg/mL), cinnamaldehyde (5 μg/mL), the combination of either compound with LPS, and the untreated condition (control). Points represent individual replicates from four independent assays. Asterisks indicate significant differences relative to the corresponding control condition (∗ P = 0.01, ∗∗ P < 0.001).

Journal: International Journal for Parasitology: Drugs and Drug Resistance

Article Title: Terpenic compounds possess anthelmintic and immunomodulatory properties with potential for controlling equine cyathostomin infections

doi: 10.1016/j.ijpddr.2026.100642

Figure Lengend Snippet: Anti-inflammatory activity of carvacrol and cinnamaldehyde on equine PBMC Boxplots showing TNF-α concentrations (ng/mL) measured in equine peripheral blood mononuclear cells (PBMCs) exposed to DMSO (0.05%), LPS (125 ng/mL), the combination of DMSO and LPS, carvacrol (5 μg/mL), cinnamaldehyde (5 μg/mL), the combination of either compound with LPS, and the untreated condition (control). Points represent individual replicates from four independent assays. Asterisks indicate significant differences relative to the corresponding control condition (∗ P = 0.01, ∗∗ P < 0.001).

Article Snippet: The cells were then incubated at +37 °C (5% CO 2 ) for 24 h. After incubation, the concentration of TNF-α in the medium for each condition was quantified by ELISA using mouse TNF-α paired antibodies (R and D Systems DY410).

Techniques: Activity Assay, Control

circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: For mouse experiments, mouse IL-10 was measured using the Mouse IL-10 ELISA Kit (R&D Systems, Cat# M1000B), and mouse TGF-β1 was measured using the Mouse TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS608-4), following the manufacturers’ instructions.

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and IL-10, and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).

Journal: Bioactive Materials

Article Title: Glucose/ROS-responsive and redox-gated adaptive hydrogel dressing for accelerating diabetic wound repair via synergistic cGAS/STING pathway inhibition and oxidative stress alleviation

doi: 10.1016/j.bioactmat.2026.03.025

Figure Lengend Snippet: Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and IL-10, and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).

Article Snippet: IL-6 and IL-10-specific antibodies were purchased from Bosterbio (Wuhan, China).

Techniques: Immunofluorescence, Staining, Fluorescence

HFD leads to downregulation of the expression of adipose Cfd and hepatic C3 and Cfb (A and B) C3-tdTomato reporter mice were placed on LFD or HFD, and expression of inflammatory markers and complement genes were assessed by qPCR in (A) subcutaneous inguinal adipose tissue and (B) visceral epididymal adipose tissue. (C) Western blot for FD in serum from female LFD and HFD mice after 25 weeks of diet. (D) Western blot for FD in serum from male mice after 15 weeks of diet. (E) Left: representative western blot from sequential serum samples from 2 male mice on HFD. Right: densitometry for serum FD signal in western blots of 6 male mice over time. (F–H) Serum FD levels, measured by ELISA, plotted against individual mouse body weight (F), fasting insulin (G), and fasting blood glucose levels (H). (I) Expression of main alternative pathway components in livers of LFD and HFD mice. (J) Protein levels of C3 in liver homogenates from lean control or ob/ob mice on the C57Bl/6 background. WAT, white adipose tissue. In (A)–(C), there were 4 mice per group, except for HFD visceral fat pad, which had 3 samples. In (F)–(H), measurements are from a total of 42 individual mouse samples. For (I) and (J), there were 4–5 mice per group. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA. See also .

Journal: iScience

Article Title: Type 2 and type 1 diabetes have opposing effects on the systemic murine complement alternative pathway

doi: 10.1016/j.isci.2026.116359

Figure Lengend Snippet: HFD leads to downregulation of the expression of adipose Cfd and hepatic C3 and Cfb (A and B) C3-tdTomato reporter mice were placed on LFD or HFD, and expression of inflammatory markers and complement genes were assessed by qPCR in (A) subcutaneous inguinal adipose tissue and (B) visceral epididymal adipose tissue. (C) Western blot for FD in serum from female LFD and HFD mice after 25 weeks of diet. (D) Western blot for FD in serum from male mice after 15 weeks of diet. (E) Left: representative western blot from sequential serum samples from 2 male mice on HFD. Right: densitometry for serum FD signal in western blots of 6 male mice over time. (F–H) Serum FD levels, measured by ELISA, plotted against individual mouse body weight (F), fasting insulin (G), and fasting blood glucose levels (H). (I) Expression of main alternative pathway components in livers of LFD and HFD mice. (J) Protein levels of C3 in liver homogenates from lean control or ob/ob mice on the C57Bl/6 background. WAT, white adipose tissue. In (A)–(C), there were 4 mice per group, except for HFD visceral fat pad, which had 3 samples. In (F)–(H), measurements are from a total of 42 individual mouse samples. For (I) and (J), there were 4–5 mice per group. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA. See also .

Article Snippet: Serum insulin was measured using an ultrasensitive mouse insulin ELISA (Mercodia #10-1249) and mouse C3b was measured in serum samples using an ELISA kit from Hycult Biotech (HK216).

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

Expression changes in STZ-induced diabetes leads to increased complement in serum and increased alternative pathway activation (A) Serum levels of FD in untreated and STZ-treated male mice. (B) Serum C3 levels in untreated controls and STZ-treated male mice. (C) Western blot for FD in homogenates of inguinal adipose tissue from control mice and STZ-treated WT and C3-KO mice. Densitometry quantification shown on the right. (D) Blood glucose levels in STZ-treated WT or C3-KO male mice over time. (E) Serum FB levels in STZ-treated male mice before and after treatment. (F) Western blot for FB in serum samples of untreated and STZ-treated male mice (top), and quantification by densitometry (bottom). (G) Example flow cytometry histograms of C3 staining of zymosan beads after incubation with serum from untreated or STZ-treated cage-mate mice in EGTA buffer, allowing only AP activation. EDTA completely inhibits complement and acts as a negative control. (H) Results of C3 deposition onto zymosan beads from serum taken at different time points from untreated or STZ-treated male mice. (I) Serum C3b levels in STZ-treated or mock-treated male mice and in STZ-treated C3-KO controls, as measured by ELISA. For all images, n = 4 untreated mice and 5 STZ-treated mice, as in , except for (C), with groups of 4; (D), with groups as stated in the figure; and (I), with n = 8, 9, and 4 for untreated, STZ-treated, and STZ-treated KO groups, respectively. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA, t test (E), or one-way ANOVA (C and I).

Journal: iScience

Article Title: Type 2 and type 1 diabetes have opposing effects on the systemic murine complement alternative pathway

doi: 10.1016/j.isci.2026.116359

Figure Lengend Snippet: Expression changes in STZ-induced diabetes leads to increased complement in serum and increased alternative pathway activation (A) Serum levels of FD in untreated and STZ-treated male mice. (B) Serum C3 levels in untreated controls and STZ-treated male mice. (C) Western blot for FD in homogenates of inguinal adipose tissue from control mice and STZ-treated WT and C3-KO mice. Densitometry quantification shown on the right. (D) Blood glucose levels in STZ-treated WT or C3-KO male mice over time. (E) Serum FB levels in STZ-treated male mice before and after treatment. (F) Western blot for FB in serum samples of untreated and STZ-treated male mice (top), and quantification by densitometry (bottom). (G) Example flow cytometry histograms of C3 staining of zymosan beads after incubation with serum from untreated or STZ-treated cage-mate mice in EGTA buffer, allowing only AP activation. EDTA completely inhibits complement and acts as a negative control. (H) Results of C3 deposition onto zymosan beads from serum taken at different time points from untreated or STZ-treated male mice. (I) Serum C3b levels in STZ-treated or mock-treated male mice and in STZ-treated C3-KO controls, as measured by ELISA. For all images, n = 4 untreated mice and 5 STZ-treated mice, as in , except for (C), with groups of 4; (D), with groups as stated in the figure; and (I), with n = 8, 9, and 4 for untreated, STZ-treated, and STZ-treated KO groups, respectively. Data represent mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by two-way ANOVA, t test (E), or one-way ANOVA (C and I).

Article Snippet: Serum insulin was measured using an ultrasensitive mouse insulin ELISA (Mercodia #10-1249) and mouse C3b was measured in serum samples using an ELISA kit from Hycult Biotech (HK216).

Techniques: Expressing, Activation Assay, Western Blot, Control, Flow Cytometry, Staining, Incubation, Negative Control, Enzyme-linked Immunosorbent Assay

T1D Akita mice have increased serum FB levels and alternative pathway activation (A) Serum FD levels in Akita and WT littermates, as measured by ELISA. (B) Serum C3 levels in the same mice. (C) Serum C3 levels in “young” versus “older” mice. (D) Serum FB levels in all Akita and WT littermate mice. (E) Serum FB levels in the same mice, stratified over time, plotting line of best fit and 95% confidence intervals. (F) C3 alternative pathway deposition onto zymosan beads from age-matched Akita or WT littermate mice. Left: example histograms from cage-mate mice; right: quantification of C3 deposition results from serum taken from age-matched pairs of mice aged from 18 to 24 weeks ( n = 5 per genotype). Each data point represents mean value from an individual mouse. Data represent mean ± SD, with ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by one-way ANOVA (F) or t test (C and D). In (E), lines show best fit and 95% confidence intervals.

Journal: iScience

Article Title: Type 2 and type 1 diabetes have opposing effects on the systemic murine complement alternative pathway

doi: 10.1016/j.isci.2026.116359

Figure Lengend Snippet: T1D Akita mice have increased serum FB levels and alternative pathway activation (A) Serum FD levels in Akita and WT littermates, as measured by ELISA. (B) Serum C3 levels in the same mice. (C) Serum C3 levels in “young” versus “older” mice. (D) Serum FB levels in all Akita and WT littermate mice. (E) Serum FB levels in the same mice, stratified over time, plotting line of best fit and 95% confidence intervals. (F) C3 alternative pathway deposition onto zymosan beads from age-matched Akita or WT littermate mice. Left: example histograms from cage-mate mice; right: quantification of C3 deposition results from serum taken from age-matched pairs of mice aged from 18 to 24 weeks ( n = 5 per genotype). Each data point represents mean value from an individual mouse. Data represent mean ± SD, with ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, as tested by one-way ANOVA (F) or t test (C and D). In (E), lines show best fit and 95% confidence intervals.

Article Snippet: Serum insulin was measured using an ultrasensitive mouse insulin ELISA (Mercodia #10-1249) and mouse C3b was measured in serum samples using an ELISA kit from Hycult Biotech (HK216).

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay