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Caliper Life Sciences fluorescence in vivo imaging system
Characterization of M2-exo@HI. (a) Western blot of Tsg101, CD9, and Calnexin expressions in RAW264.7 and M2-exo. (b) Protein bands of RAW264.7, M2-exo, M2-exo@HI, and HI by SDS-PAGE. (c) <t>Fluorescence</t> microscopy images showing Hp-EGFP and IL-10-mCherry expression in 293T cells infected with lipo2000@pBudCE4.1 , lipo2000@HI, and M2-exo@HI respectively, after 24 h. (d,e) Representative TEM images and size distribution profiles of M2-exo and M2-exo@HI. (f) Particle number of M2-exo and M2-exo@HI by NTA measurement. (g) Zeta potentials of M2-exo and M2-exo@HI (n = 3). (h) Drug release profiles of M2-exo@HI at pH 6.5 and pH 7.4, respectively (n = 3). (i) Stability evaluation of M2-exo@HI in PBS at 4 °C by monitoring particle size over time (n = 3). Data are presented as mean ± SD.
Fluorescence In Vivo Imaging System, supplied by Caliper Life Sciences, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage"

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.01.047

Characterization of M2-exo@HI. (a) Western blot of Tsg101, CD9, and Calnexin expressions in RAW264.7 and M2-exo. (b) Protein bands of RAW264.7, M2-exo, M2-exo@HI, and HI by SDS-PAGE. (c) Fluorescence microscopy images showing Hp-EGFP and IL-10-mCherry expression in 293T cells infected with lipo2000@pBudCE4.1 , lipo2000@HI, and M2-exo@HI respectively, after 24 h. (d,e) Representative TEM images and size distribution profiles of M2-exo and M2-exo@HI. (f) Particle number of M2-exo and M2-exo@HI by NTA measurement. (g) Zeta potentials of M2-exo and M2-exo@HI (n = 3). (h) Drug release profiles of M2-exo@HI at pH 6.5 and pH 7.4, respectively (n = 3). (i) Stability evaluation of M2-exo@HI in PBS at 4 °C by monitoring particle size over time (n = 3). Data are presented as mean ± SD.
Figure Legend Snippet: Characterization of M2-exo@HI. (a) Western blot of Tsg101, CD9, and Calnexin expressions in RAW264.7 and M2-exo. (b) Protein bands of RAW264.7, M2-exo, M2-exo@HI, and HI by SDS-PAGE. (c) Fluorescence microscopy images showing Hp-EGFP and IL-10-mCherry expression in 293T cells infected with lipo2000@pBudCE4.1 , lipo2000@HI, and M2-exo@HI respectively, after 24 h. (d,e) Representative TEM images and size distribution profiles of M2-exo and M2-exo@HI. (f) Particle number of M2-exo and M2-exo@HI by NTA measurement. (g) Zeta potentials of M2-exo and M2-exo@HI (n = 3). (h) Drug release profiles of M2-exo@HI at pH 6.5 and pH 7.4, respectively (n = 3). (i) Stability evaluation of M2-exo@HI in PBS at 4 °C by monitoring particle size over time (n = 3). Data are presented as mean ± SD.

Techniques Used: Western Blot, SDS Page, Fluorescence, Microscopy, Expressing, Infection

Validation of M2-exo targeting, Hp/IL-10 transfection expression, and Hp/Hb binding. (a) Fluorescence imaging showing cellular uptake of ICG and M2-exo@ICG by M1 microglia. (b,c) Flow cytometry and corresponding quantification of RhB and M2-exo@RhB internalized by M1 microglia (n = 3). (d,e) Schematic illustration and quantitative analysis of the in vitro phagocytosis-release kinetics of M2-exo@RhB in BV2 under ICH-mimicking stimulation (n = 6). (f) Fluorescence images showing Hp and IL-10 expression in M1 microglia treated with M2-exo@HI for 12, 24, 48, 72 h. (g) Mean fluorescence intensity (MFI) quantification of Hp and IL-10 expression (n = 3). (h,i) ELISA measurements of secreted Hp and IL-10 protein levels (n = 3). (j,k) qPCR analysis of relative Hp and IL-10 mRNA expression (n = 3). (l) Western blot detection of Hp and IL-10 protein expression. (m) Densitometric quantification of Hp and IL-10 protein levels from Western blot (n = 3). (n) Co-immunoprecipitation assay confirming the formation of Hp-Hb complex. Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (c and e), and one-way ANOVA with Tukey's multiple comparisons test (g-k and m).
Figure Legend Snippet: Validation of M2-exo targeting, Hp/IL-10 transfection expression, and Hp/Hb binding. (a) Fluorescence imaging showing cellular uptake of ICG and M2-exo@ICG by M1 microglia. (b,c) Flow cytometry and corresponding quantification of RhB and M2-exo@RhB internalized by M1 microglia (n = 3). (d,e) Schematic illustration and quantitative analysis of the in vitro phagocytosis-release kinetics of M2-exo@RhB in BV2 under ICH-mimicking stimulation (n = 6). (f) Fluorescence images showing Hp and IL-10 expression in M1 microglia treated with M2-exo@HI for 12, 24, 48, 72 h. (g) Mean fluorescence intensity (MFI) quantification of Hp and IL-10 expression (n = 3). (h,i) ELISA measurements of secreted Hp and IL-10 protein levels (n = 3). (j,k) qPCR analysis of relative Hp and IL-10 mRNA expression (n = 3). (l) Western blot detection of Hp and IL-10 protein expression. (m) Densitometric quantification of Hp and IL-10 protein levels from Western blot (n = 3). (n) Co-immunoprecipitation assay confirming the formation of Hp-Hb complex. Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (c and e), and one-way ANOVA with Tukey's multiple comparisons test (g-k and m).

Techniques Used: Biomarker Discovery, Transfection, Expressing, Binding Assay, Fluorescence, Imaging, Flow Cytometry, In Vitro, Enzyme-linked Immunosorbent Assay, Western Blot, Co-Immunoprecipitation Assay

M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.
Figure Legend Snippet: M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

Techniques Used: In Vitro, Flow Cytometry, Fluorescence, Microscopy, Permeability, Transwell Assay

Targeted delivery and therapeutic gene expression of M2-exo@HI in hemorrhagic brain. (a) In vivo near-infrared fluorescence imaging showing ICG and M2-exo@ICG in mouse brains at various time points post-injection. (b) Average radiation efficiency of ICG in different treatment groups (n = 3). (c) Ex vivo fluorescence imaging of major organs harvested 24 h post-injection. (d) Average radiation efficiency of ICG in different in mouse tissues (n = 3). (e) Time-dependent accumulation of M2-exo@ICG at hematoma regions. (f) Immunofluorescence staining showing co-localization of Hp/IL-10 with astrocytes, microglia, and endothelial cells. (g) Temporal expression profiles of Hp and IL-10 in brain tissues. (h,i) ELISA quantification of Hp and IL-10 protein levels in brain homogenates (n = 3). Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (b,d), and one-way ANOVA with Tukey's multiple comparisons test (h,i).
Figure Legend Snippet: Targeted delivery and therapeutic gene expression of M2-exo@HI in hemorrhagic brain. (a) In vivo near-infrared fluorescence imaging showing ICG and M2-exo@ICG in mouse brains at various time points post-injection. (b) Average radiation efficiency of ICG in different treatment groups (n = 3). (c) Ex vivo fluorescence imaging of major organs harvested 24 h post-injection. (d) Average radiation efficiency of ICG in different in mouse tissues (n = 3). (e) Time-dependent accumulation of M2-exo@ICG at hematoma regions. (f) Immunofluorescence staining showing co-localization of Hp/IL-10 with astrocytes, microglia, and endothelial cells. (g) Temporal expression profiles of Hp and IL-10 in brain tissues. (h,i) ELISA quantification of Hp and IL-10 protein levels in brain homogenates (n = 3). Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (b,d), and one-way ANOVA with Tukey's multiple comparisons test (h,i).

Techniques Used: Gene Expression, In Vivo, Fluorescence, Imaging, Injection, Ex Vivo, Immunofluorescence, Staining, Expressing, Enzyme-linked Immunosorbent Assay



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Characterization of M2-exo@HI. (a) Western blot of Tsg101, CD9, and Calnexin expressions in RAW264.7 and M2-exo. (b) Protein bands of RAW264.7, M2-exo, M2-exo@HI, and HI by SDS-PAGE. (c) <t>Fluorescence</t> microscopy images showing Hp-EGFP and IL-10-mCherry expression in 293T cells infected with lipo2000@pBudCE4.1 , lipo2000@HI, and M2-exo@HI respectively, after 24 h. (d,e) Representative TEM images and size distribution profiles of M2-exo and M2-exo@HI. (f) Particle number of M2-exo and M2-exo@HI by NTA measurement. (g) Zeta potentials of M2-exo and M2-exo@HI (n = 3). (h) Drug release profiles of M2-exo@HI at pH 6.5 and pH 7.4, respectively (n = 3). (i) Stability evaluation of M2-exo@HI in PBS at 4 °C by monitoring particle size over time (n = 3). Data are presented as mean ± SD.
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Image Search Results


Alcohol consumption aggravates prostate inflammation and promotes M1 macrophage polarization in EAP mice. ( A ) Schematic of the experimental timeline for EAP induction and alcohol intervention. ( B ) The body weights of mice in the Control, Control+Alcohol, EAP, and EAP+Alcohol groups. ( C and D ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( E ) Prostate inflammation score. ( F ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( G ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( H ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( I-J ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( K ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. Data are presented as mean ± SD (n = 6 for B-K). *, p < 0.05; ***, p < 0.001.

Journal: International Journal of Nanomedicine

Article Title: Lactobacillus johnsonii -Derived Extracellular Vesicles Ameliorate Alcohol-Exacerbated Experimental Autoimmune Prostatitis by Inhibiting M1 Macrophage Polarization

doi: 10.2147/IJN.S596237

Figure Lengend Snippet: Alcohol consumption aggravates prostate inflammation and promotes M1 macrophage polarization in EAP mice. ( A ) Schematic of the experimental timeline for EAP induction and alcohol intervention. ( B ) The body weights of mice in the Control, Control+Alcohol, EAP, and EAP+Alcohol groups. ( C and D ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( E ) Prostate inflammation score. ( F ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( G ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( H ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( I-J ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( K ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. Data are presented as mean ± SD (n = 6 for B-K). *, p < 0.05; ***, p < 0.001.

Article Snippet: The in vivo fluorescence distribution was evaluated 12 hours post-injection using an imaging system from MILabs (Netherlands).

Techniques: Control, Staining, Immunohistochemistry, Immunohistochemical staining, Fluorescence, Immunofluorescence

The gut microbiota mediates the effect of alcohol on EAP mice. ( A and B ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( C ) Prostate inflammation score. ( D ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( E ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( F ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( G ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. ( H ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( I ) Pro-inflammatory cytokine levels in serum. ( J ) Pro-inflammatory cytokine mRNA expression in prostate tissues. Data are presented as mean ± SD (n = 6 for A-I, n = 4 for J). *, p < 0.05; **, p < 0.01; ***, p < 0.001.

Journal: International Journal of Nanomedicine

Article Title: Lactobacillus johnsonii -Derived Extracellular Vesicles Ameliorate Alcohol-Exacerbated Experimental Autoimmune Prostatitis by Inhibiting M1 Macrophage Polarization

doi: 10.2147/IJN.S596237

Figure Lengend Snippet: The gut microbiota mediates the effect of alcohol on EAP mice. ( A and B ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( C ) Prostate inflammation score. ( D ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( E ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( F ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( G ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. ( H ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( I ) Pro-inflammatory cytokine levels in serum. ( J ) Pro-inflammatory cytokine mRNA expression in prostate tissues. Data are presented as mean ± SD (n = 6 for A-I, n = 4 for J). *, p < 0.05; **, p < 0.01; ***, p < 0.001.

Article Snippet: The in vivo fluorescence distribution was evaluated 12 hours post-injection using an imaging system from MILabs (Netherlands).

Techniques: Staining, Immunohistochemical staining, Immunohistochemistry, Immunofluorescence, Fluorescence, Expressing

Transplantation of L. john relieves prostate inflammation and pain in EAP mice. ( A and B ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( C ) Prostate inflammation score. ( D ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( E ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( F ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( G-H ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( I ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. Data are presented as mean ± SD (n = 6 for A-I). *, p < 0.05; **, p < 0.01.

Journal: International Journal of Nanomedicine

Article Title: Lactobacillus johnsonii -Derived Extracellular Vesicles Ameliorate Alcohol-Exacerbated Experimental Autoimmune Prostatitis by Inhibiting M1 Macrophage Polarization

doi: 10.2147/IJN.S596237

Figure Lengend Snippet: Transplantation of L. john relieves prostate inflammation and pain in EAP mice. ( A and B ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( C ) Prostate inflammation score. ( D ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( E ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( F ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( G-H ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( I ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. Data are presented as mean ± SD (n = 6 for A-I). *, p < 0.05; **, p < 0.01.

Article Snippet: The in vivo fluorescence distribution was evaluated 12 hours post-injection using an imaging system from MILabs (Netherlands).

Techniques: Transplantation Assay, Staining, Immunohistochemistry, Immunohistochemical staining, Fluorescence, Immunofluorescence

LjEVs alleviate prostate inflammation and inhibit M1 macrophage polarization in EAP mice. ( A ) Transmission electron microscopy (TEM) image of LjEVs. Scale bars, 100 nm. ( B and C ) Size distribution and concentration of LjEVs analyzed by nano-flow cytometry (nFCM). ( D and E ) The biodistribution of EVs@ICG versus free ICG was assessed in vivo and ex vivo after administration via tail vein injection. ( F and G ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( H ) Prostate inflammation score. ( I ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( J ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( K ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( L ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. ( M ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( N ) Pro-inflammatory cytokine levels in serum. ( O ) Pro-inflammatory cytokine mRNA expression in prostate tissues. Data are presented as mean ± SD (n = 6 for F-N, n = 4 for O). *, p < 0.05; **, p < 0.01; ***, p < 0.001.

Journal: International Journal of Nanomedicine

Article Title: Lactobacillus johnsonii -Derived Extracellular Vesicles Ameliorate Alcohol-Exacerbated Experimental Autoimmune Prostatitis by Inhibiting M1 Macrophage Polarization

doi: 10.2147/IJN.S596237

Figure Lengend Snippet: LjEVs alleviate prostate inflammation and inhibit M1 macrophage polarization in EAP mice. ( A ) Transmission electron microscopy (TEM) image of LjEVs. Scale bars, 100 nm. ( B and C ) Size distribution and concentration of LjEVs analyzed by nano-flow cytometry (nFCM). ( D and E ) The biodistribution of EVs@ICG versus free ICG was assessed in vivo and ex vivo after administration via tail vein injection. ( F and G ) Response frequency to mechanical stimuli and the 50% mechanical withdrawal threshold. ( H ) Prostate inflammation score. ( I ) H&E staining of the anterior and dorsolateral prostate. Scale bars, 100 μm. ( J ) Immunohistochemical staining of CD45 in prostate tissues. Scale bars, 100 μm. ( K ) Percentage of CD45-positive staining in prostate immunohistochemistry. ( L ) Immunofluorescence staining of CD86 and CD206 in prostate tissue. Scale bars, 50 μm. ( M ) Relative fluorescence intensity of CD86 and CD206 in prostate tissue. ( N ) Pro-inflammatory cytokine levels in serum. ( O ) Pro-inflammatory cytokine mRNA expression in prostate tissues. Data are presented as mean ± SD (n = 6 for F-N, n = 4 for O). *, p < 0.05; **, p < 0.01; ***, p < 0.001.

Article Snippet: The in vivo fluorescence distribution was evaluated 12 hours post-injection using an imaging system from MILabs (Netherlands).

Techniques: Transmission Assay, Electron Microscopy, Concentration Assay, Flow Cytometry, In Vivo, Ex Vivo, Injection, Staining, Immunohistochemical staining, Immunohistochemistry, Immunofluorescence, Fluorescence, Expressing

Characterization of M2-exo@HI. (a) Western blot of Tsg101, CD9, and Calnexin expressions in RAW264.7 and M2-exo. (b) Protein bands of RAW264.7, M2-exo, M2-exo@HI, and HI by SDS-PAGE. (c) Fluorescence microscopy images showing Hp-EGFP and IL-10-mCherry expression in 293T cells infected with lipo2000@pBudCE4.1 , lipo2000@HI, and M2-exo@HI respectively, after 24 h. (d,e) Representative TEM images and size distribution profiles of M2-exo and M2-exo@HI. (f) Particle number of M2-exo and M2-exo@HI by NTA measurement. (g) Zeta potentials of M2-exo and M2-exo@HI (n = 3). (h) Drug release profiles of M2-exo@HI at pH 6.5 and pH 7.4, respectively (n = 3). (i) Stability evaluation of M2-exo@HI in PBS at 4 °C by monitoring particle size over time (n = 3). Data are presented as mean ± SD.

Journal: Bioactive Materials

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

doi: 10.1016/j.bioactmat.2026.01.047

Figure Lengend Snippet: Characterization of M2-exo@HI. (a) Western blot of Tsg101, CD9, and Calnexin expressions in RAW264.7 and M2-exo. (b) Protein bands of RAW264.7, M2-exo, M2-exo@HI, and HI by SDS-PAGE. (c) Fluorescence microscopy images showing Hp-EGFP and IL-10-mCherry expression in 293T cells infected with lipo2000@pBudCE4.1 , lipo2000@HI, and M2-exo@HI respectively, after 24 h. (d,e) Representative TEM images and size distribution profiles of M2-exo and M2-exo@HI. (f) Particle number of M2-exo and M2-exo@HI by NTA measurement. (g) Zeta potentials of M2-exo and M2-exo@HI (n = 3). (h) Drug release profiles of M2-exo@HI at pH 6.5 and pH 7.4, respectively (n = 3). (i) Stability evaluation of M2-exo@HI in PBS at 4 °C by monitoring particle size over time (n = 3). Data are presented as mean ± SD.

Article Snippet: Then mice were anesthetized with 5 % isoflurane and imaged using near-infrared fluorescence in vivo imaging system (IVIS, Caliper Life Sciences, USA) at predetermined time intervals (1 min, 5 min, 10 min, 15min, 2 h, 6 h, 12 h, 24 h).

Techniques: Western Blot, SDS Page, Fluorescence, Microscopy, Expressing, Infection

Validation of M2-exo targeting, Hp/IL-10 transfection expression, and Hp/Hb binding. (a) Fluorescence imaging showing cellular uptake of ICG and M2-exo@ICG by M1 microglia. (b,c) Flow cytometry and corresponding quantification of RhB and M2-exo@RhB internalized by M1 microglia (n = 3). (d,e) Schematic illustration and quantitative analysis of the in vitro phagocytosis-release kinetics of M2-exo@RhB in BV2 under ICH-mimicking stimulation (n = 6). (f) Fluorescence images showing Hp and IL-10 expression in M1 microglia treated with M2-exo@HI for 12, 24, 48, 72 h. (g) Mean fluorescence intensity (MFI) quantification of Hp and IL-10 expression (n = 3). (h,i) ELISA measurements of secreted Hp and IL-10 protein levels (n = 3). (j,k) qPCR analysis of relative Hp and IL-10 mRNA expression (n = 3). (l) Western blot detection of Hp and IL-10 protein expression. (m) Densitometric quantification of Hp and IL-10 protein levels from Western blot (n = 3). (n) Co-immunoprecipitation assay confirming the formation of Hp-Hb complex. Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (c and e), and one-way ANOVA with Tukey's multiple comparisons test (g-k and m).

Journal: Bioactive Materials

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

doi: 10.1016/j.bioactmat.2026.01.047

Figure Lengend Snippet: Validation of M2-exo targeting, Hp/IL-10 transfection expression, and Hp/Hb binding. (a) Fluorescence imaging showing cellular uptake of ICG and M2-exo@ICG by M1 microglia. (b,c) Flow cytometry and corresponding quantification of RhB and M2-exo@RhB internalized by M1 microglia (n = 3). (d,e) Schematic illustration and quantitative analysis of the in vitro phagocytosis-release kinetics of M2-exo@RhB in BV2 under ICH-mimicking stimulation (n = 6). (f) Fluorescence images showing Hp and IL-10 expression in M1 microglia treated with M2-exo@HI for 12, 24, 48, 72 h. (g) Mean fluorescence intensity (MFI) quantification of Hp and IL-10 expression (n = 3). (h,i) ELISA measurements of secreted Hp and IL-10 protein levels (n = 3). (j,k) qPCR analysis of relative Hp and IL-10 mRNA expression (n = 3). (l) Western blot detection of Hp and IL-10 protein expression. (m) Densitometric quantification of Hp and IL-10 protein levels from Western blot (n = 3). (n) Co-immunoprecipitation assay confirming the formation of Hp-Hb complex. Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (c and e), and one-way ANOVA with Tukey's multiple comparisons test (g-k and m).

Article Snippet: Then mice were anesthetized with 5 % isoflurane and imaged using near-infrared fluorescence in vivo imaging system (IVIS, Caliper Life Sciences, USA) at predetermined time intervals (1 min, 5 min, 10 min, 15min, 2 h, 6 h, 12 h, 24 h).

Techniques: Biomarker Discovery, Transfection, Expressing, Binding Assay, Fluorescence, Imaging, Flow Cytometry, In Vitro, Enzyme-linked Immunosorbent Assay, Western Blot, Co-Immunoprecipitation Assay

M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

Journal: Bioactive Materials

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

doi: 10.1016/j.bioactmat.2026.01.047

Figure Lengend Snippet: M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

Article Snippet: Then mice were anesthetized with 5 % isoflurane and imaged using near-infrared fluorescence in vivo imaging system (IVIS, Caliper Life Sciences, USA) at predetermined time intervals (1 min, 5 min, 10 min, 15min, 2 h, 6 h, 12 h, 24 h).

Techniques: In Vitro, Flow Cytometry, Fluorescence, Microscopy, Permeability, Transwell Assay

Targeted delivery and therapeutic gene expression of M2-exo@HI in hemorrhagic brain. (a) In vivo near-infrared fluorescence imaging showing ICG and M2-exo@ICG in mouse brains at various time points post-injection. (b) Average radiation efficiency of ICG in different treatment groups (n = 3). (c) Ex vivo fluorescence imaging of major organs harvested 24 h post-injection. (d) Average radiation efficiency of ICG in different in mouse tissues (n = 3). (e) Time-dependent accumulation of M2-exo@ICG at hematoma regions. (f) Immunofluorescence staining showing co-localization of Hp/IL-10 with astrocytes, microglia, and endothelial cells. (g) Temporal expression profiles of Hp and IL-10 in brain tissues. (h,i) ELISA quantification of Hp and IL-10 protein levels in brain homogenates (n = 3). Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (b,d), and one-way ANOVA with Tukey's multiple comparisons test (h,i).

Journal: Bioactive Materials

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

doi: 10.1016/j.bioactmat.2026.01.047

Figure Lengend Snippet: Targeted delivery and therapeutic gene expression of M2-exo@HI in hemorrhagic brain. (a) In vivo near-infrared fluorescence imaging showing ICG and M2-exo@ICG in mouse brains at various time points post-injection. (b) Average radiation efficiency of ICG in different treatment groups (n = 3). (c) Ex vivo fluorescence imaging of major organs harvested 24 h post-injection. (d) Average radiation efficiency of ICG in different in mouse tissues (n = 3). (e) Time-dependent accumulation of M2-exo@ICG at hematoma regions. (f) Immunofluorescence staining showing co-localization of Hp/IL-10 with astrocytes, microglia, and endothelial cells. (g) Temporal expression profiles of Hp and IL-10 in brain tissues. (h,i) ELISA quantification of Hp and IL-10 protein levels in brain homogenates (n = 3). Data are presented as mean ± SD. Statistical significance was calculated by unpaired Student's t -test (b,d), and one-way ANOVA with Tukey's multiple comparisons test (h,i).

Article Snippet: Then mice were anesthetized with 5 % isoflurane and imaged using near-infrared fluorescence in vivo imaging system (IVIS, Caliper Life Sciences, USA) at predetermined time intervals (1 min, 5 min, 10 min, 15min, 2 h, 6 h, 12 h, 24 h).

Techniques: Gene Expression, In Vivo, Fluorescence, Imaging, Injection, Ex Vivo, Immunofluorescence, Staining, Expressing, Enzyme-linked Immunosorbent Assay

(A) Chemical structure of SPP. The red part represents toxicity payload SN38; The blue part represents the GSH responsive linker disulfide bond; The black part represents the spacer PEG 24 ; The green part represents the specific PSMA targeting ligand. (B) The LC-MS characterization results of SPP. (C) The UV–vis absorption spectrum and the fluorescence emission spectrum of SPP (in DMSO, Ex = 365 nm, Em = 430 nm). (D) HPLC analysis of SPP before and after incubation with GSH (5 μM). (E) HPLC analysis of SPP before and after incubation with GSH (5 mM). (F) HPLC analysis of CPP before and after incubation with GSH (5 mM). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: International Journal of Pharmaceutics: X

Article Title: A prostate-specific membrane antigen targeted small molecule-drug conjugate for efficient prostate cancer therapy at a low dosage

doi: 10.1016/j.ijpx.2026.100496

Figure Lengend Snippet: (A) Chemical structure of SPP. The red part represents toxicity payload SN38; The blue part represents the GSH responsive linker disulfide bond; The black part represents the spacer PEG 24 ; The green part represents the specific PSMA targeting ligand. (B) The LC-MS characterization results of SPP. (C) The UV–vis absorption spectrum and the fluorescence emission spectrum of SPP (in DMSO, Ex = 365 nm, Em = 430 nm). (D) HPLC analysis of SPP before and after incubation with GSH (5 μM). (E) HPLC analysis of SPP before and after incubation with GSH (5 mM). (F) HPLC analysis of CPP before and after incubation with GSH (5 mM). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: In vivo fluorescence imaging was performed at several time points (0.5 h, 1 h, 2 h and 4 h) post intravenous injection using a living animal imaging system (VISQUE In Vivo Optical Imager, Vieworks, Korea, Cy5.5 emission channel).

Techniques: Liquid Chromatography with Mass Spectroscopy, Fluorescence, Incubation

(A) Fluorescence imaging of tumor-bearing mice after tail vein injection of PHA-SS-3PEG 24 -3PSMA (20 nmol, 200 μL) at different times. The white circles indicate the tumors. (B) Semi-quantitative fluorescence signal analysis of the tumor site at different time points. (C) Representative fluorescence imaging of major organs, tumors and muscle adjacent to the tumor at 1, 2 and 4 h post administration of PHA-SS-3PEG 24 -3PSMA. H-heart, Li-liver, Sp-spleen, Lu-lung, K-kidney, St-stomach, I-intestine, T-tumor, and N-normal muscle. (D) Semi-quantitative analysis of biodistribution 4 h post injection of SPP in (C).

Journal: International Journal of Pharmaceutics: X

Article Title: A prostate-specific membrane antigen targeted small molecule-drug conjugate for efficient prostate cancer therapy at a low dosage

doi: 10.1016/j.ijpx.2026.100496

Figure Lengend Snippet: (A) Fluorescence imaging of tumor-bearing mice after tail vein injection of PHA-SS-3PEG 24 -3PSMA (20 nmol, 200 μL) at different times. The white circles indicate the tumors. (B) Semi-quantitative fluorescence signal analysis of the tumor site at different time points. (C) Representative fluorescence imaging of major organs, tumors and muscle adjacent to the tumor at 1, 2 and 4 h post administration of PHA-SS-3PEG 24 -3PSMA. H-heart, Li-liver, Sp-spleen, Lu-lung, K-kidney, St-stomach, I-intestine, T-tumor, and N-normal muscle. (D) Semi-quantitative analysis of biodistribution 4 h post injection of SPP in (C).

Article Snippet: In vivo fluorescence imaging was performed at several time points (0.5 h, 1 h, 2 h and 4 h) post intravenous injection using a living animal imaging system (VISQUE In Vivo Optical Imager, Vieworks, Korea, Cy5.5 emission channel).

Techniques: Fluorescence, Imaging, Injection

(A) Scheme of in vivo antitumor therapy. (B) photos of tumor-bearing mice in different groups after 10 days' treatments. (C) Tumor growth curves of mice in different groups during 10 days' treatments. Group 1: Control; Group 2: CPP; Group 3: SN38-SS-3PEG 24 ; Group 4: SN38-CC-3PEG 24 -3PSMA; Group 5: SPP. (D) Statistics of tumor weights collected from mice on the 10th day. (E) Body weight changes of tumor-bearing mice during the treatments. Statistical significance was calculated by t -test with GraphPad, ** p < 0.01, * p < 0.05. (F) Tumor slices with H&E staining from the Control group and the SPP group on 10th day after treatment. Scale bar = 100 μm. (G) Fluorescence imaging of tumor sections from the Control group and the SPP group on 10th day after treatment. Scale bar = 100 μm.

Journal: International Journal of Pharmaceutics: X

Article Title: A prostate-specific membrane antigen targeted small molecule-drug conjugate for efficient prostate cancer therapy at a low dosage

doi: 10.1016/j.ijpx.2026.100496

Figure Lengend Snippet: (A) Scheme of in vivo antitumor therapy. (B) photos of tumor-bearing mice in different groups after 10 days' treatments. (C) Tumor growth curves of mice in different groups during 10 days' treatments. Group 1: Control; Group 2: CPP; Group 3: SN38-SS-3PEG 24 ; Group 4: SN38-CC-3PEG 24 -3PSMA; Group 5: SPP. (D) Statistics of tumor weights collected from mice on the 10th day. (E) Body weight changes of tumor-bearing mice during the treatments. Statistical significance was calculated by t -test with GraphPad, ** p < 0.01, * p < 0.05. (F) Tumor slices with H&E staining from the Control group and the SPP group on 10th day after treatment. Scale bar = 100 μm. (G) Fluorescence imaging of tumor sections from the Control group and the SPP group on 10th day after treatment. Scale bar = 100 μm.

Article Snippet: In vivo fluorescence imaging was performed at several time points (0.5 h, 1 h, 2 h and 4 h) post intravenous injection using a living animal imaging system (VISQUE In Vivo Optical Imager, Vieworks, Korea, Cy5.5 emission channel).

Techniques: In Vivo, Control, Staining, Fluorescence, Imaging

Generation of bioengineered LEVs (LEVs@TA) through in situ TA modifications. ( A ) Schematic illustration showing the interaction of TA with the phospholipid bilayer of LEVs via hydrogen bonding and the uptake of LEVs@TA by macrophages. ( B ) The percentages of CY5-TA-modified cells following incubation with gradient concentrations of CY5-TA (0, 0.1, 1, 5, and 10 μM) for 24 h (flow cytometry assay). ( C ) Colocalization of CY5-TA on HEK293T cells following incubation in 10 μM CY5-TA for 24 h (fluorescence microscopy). The nuclei were stained with DAPI (blue). ( D ) The percentages of CY5-TA-modified LEVs following incubation with gradient concentrations of CY5-TA (0, 10, 20, 50, and 100 μM) for 24 h (flow cytometry assay). ( E ) Colocalization of CY5-TA and PKH67-labeled LEVs (green) following incubation with 100 μM CY5-TA for 24 h (fluorescence microscopy). ( F ) Snapshots of CGMD simulations depicting the uptake of LEVs and LEVs@TA by macrophages at 0, 5, 10, 15, and 20 ns. ( G ) Representative in vivo fluorescence images showing good stability of DIO-labeled-LEVs@CY5-TA in vivo .

Journal: Bioactive Materials

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment

doi: 10.1016/j.bioactmat.2026.01.002

Figure Lengend Snippet: Generation of bioengineered LEVs (LEVs@TA) through in situ TA modifications. ( A ) Schematic illustration showing the interaction of TA with the phospholipid bilayer of LEVs via hydrogen bonding and the uptake of LEVs@TA by macrophages. ( B ) The percentages of CY5-TA-modified cells following incubation with gradient concentrations of CY5-TA (0, 0.1, 1, 5, and 10 μM) for 24 h (flow cytometry assay). ( C ) Colocalization of CY5-TA on HEK293T cells following incubation in 10 μM CY5-TA for 24 h (fluorescence microscopy). The nuclei were stained with DAPI (blue). ( D ) The percentages of CY5-TA-modified LEVs following incubation with gradient concentrations of CY5-TA (0, 10, 20, 50, and 100 μM) for 24 h (flow cytometry assay). ( E ) Colocalization of CY5-TA and PKH67-labeled LEVs (green) following incubation with 100 μM CY5-TA for 24 h (fluorescence microscopy). ( F ) Snapshots of CGMD simulations depicting the uptake of LEVs and LEVs@TA by macrophages at 0, 5, 10, 15, and 20 ns. ( G ) Representative in vivo fluorescence images showing good stability of DIO-labeled-LEVs@CY5-TA in vivo .

Article Snippet: At different time points (6, 12, 24, and 48 h) after injection of DIO-labeled-LEVs@CY5-TA, the fluorescence distribution in vivo was visualized and imaged using an in vivo fluorescence imaging system (DIO: Ex/Em: 465/540 nm; CY5: Ex/Em: 640/700 nm; AniView100/600 DXA, Guangzhou Biolight Biotechnology, China).

Techniques: In Situ, Modification, Incubation, Flow Cytometry, Fluorescence, Microscopy, Staining, Labeling, In Vivo

Endo/lysosomal escape capacity of bioengineered LEVs@TA following uptake by macrophages. ( A ) Schematic illustration showing the endo/lysosomal escape process of LEVs@TA within the cytoplasm of macrophages. After uptake by macrophages, LEVs@TA were entrapped within endo/lysosomes, and then TA underwent protonation and disassembled from LEVs in an acidic environment, leading to rupture of the endo/lysosomal structure. ( B ) Snapshots of CGMD simulations showing the disassembly of TA and LEVs in the lysosomal environment. ( C ) Colocalization of LysoTracker-labeled endo/lysosomes (violet) and PKH67-labeled LEVs or LEVs@TA (green) (fluorescence microscopy). The nuclei were stained with Hoechst (blue). ( D ) Quantification of the colocalization of endo/lysosomes and LEVs or LEVs@TA using the Pearson correlation coefficient ( n = 12). ( E ) Schematic illustration showing the leakage of calcein into the cytosol when TA diffused from LEVs@TA and destabilized the endo/lysosomal membranes. ( F ) The distribution of calcein (green) in macrophages treated with PBS, LEVs, and LEVs@TA (fluorescence microscopy). (G) Representative TEM images of macrophages showing the structure of lysosomes in macrophages treated with LEVs and LEVs@TA. The data are expressed as the mean ± SEM. Statistical analysis was performed with Student's t -test ( D ). ∗∗∗ p < 0.001 indicates significant differences between the indicated columns.

Journal: Bioactive Materials

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment

doi: 10.1016/j.bioactmat.2026.01.002

Figure Lengend Snippet: Endo/lysosomal escape capacity of bioengineered LEVs@TA following uptake by macrophages. ( A ) Schematic illustration showing the endo/lysosomal escape process of LEVs@TA within the cytoplasm of macrophages. After uptake by macrophages, LEVs@TA were entrapped within endo/lysosomes, and then TA underwent protonation and disassembled from LEVs in an acidic environment, leading to rupture of the endo/lysosomal structure. ( B ) Snapshots of CGMD simulations showing the disassembly of TA and LEVs in the lysosomal environment. ( C ) Colocalization of LysoTracker-labeled endo/lysosomes (violet) and PKH67-labeled LEVs or LEVs@TA (green) (fluorescence microscopy). The nuclei were stained with Hoechst (blue). ( D ) Quantification of the colocalization of endo/lysosomes and LEVs or LEVs@TA using the Pearson correlation coefficient ( n = 12). ( E ) Schematic illustration showing the leakage of calcein into the cytosol when TA diffused from LEVs@TA and destabilized the endo/lysosomal membranes. ( F ) The distribution of calcein (green) in macrophages treated with PBS, LEVs, and LEVs@TA (fluorescence microscopy). (G) Representative TEM images of macrophages showing the structure of lysosomes in macrophages treated with LEVs and LEVs@TA. The data are expressed as the mean ± SEM. Statistical analysis was performed with Student's t -test ( D ). ∗∗∗ p < 0.001 indicates significant differences between the indicated columns.

Article Snippet: At different time points (6, 12, 24, and 48 h) after injection of DIO-labeled-LEVs@CY5-TA, the fluorescence distribution in vivo was visualized and imaged using an in vivo fluorescence imaging system (DIO: Ex/Em: 465/540 nm; CY5: Ex/Em: 640/700 nm; AniView100/600 DXA, Guangzhou Biolight Biotechnology, China).

Techniques: Labeling, Fluorescence, Microscopy, Staining

Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H ) JC-1 aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Journal: Bioactive Materials

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment

doi: 10.1016/j.bioactmat.2026.01.002

Figure Lengend Snippet: Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H ) JC-1 aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Article Snippet: At different time points (6, 12, 24, and 48 h) after injection of DIO-labeled-LEVs@CY5-TA, the fluorescence distribution in vivo was visualized and imaged using an in vivo fluorescence imaging system (DIO: Ex/Em: 465/540 nm; CY5: Ex/Em: 640/700 nm; AniView100/600 DXA, Guangzhou Biolight Biotechnology, China).

Techniques: Control, Fluorescence, Immunofluorescence

In vivo sustained release and cardiac function assessment. (A) Fluorescence images of HdECM, and AS-IV@HdECM (n = 3) injected in intrapericardial cavity (IPC) and (B) quantitative analysis of fluorescence signal. (C) Time-dependent concentration of released AS-IV in the serum of the treatment groups AS-IV and AS-IV@HdECM (n = 3). (D,E) Bar graphs depicting CK-MB and cTnI levels in each group (n = 5). (F) Representative echocardiographic images of different groups at 14 and 28 days post the treatment. Assessment of cardiac function parameters: (G) Left ventricular ejection fraction (LVEF), (H) Left ventricular fractional shortening (LVFS), (I) left ventricular internal diameter at end-systole (LVIDs), and (J) left ventricular internal diameter at end-diastole (LVIDd) (n = 5). All bar graphs include individual data points.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: A bioactive heart-derived ECM hydrogel potentiates Astragaloside IV–mediated microvascular regeneration

doi: 10.3389/fbioe.2026.1800990

Figure Lengend Snippet: In vivo sustained release and cardiac function assessment. (A) Fluorescence images of HdECM, and AS-IV@HdECM (n = 3) injected in intrapericardial cavity (IPC) and (B) quantitative analysis of fluorescence signal. (C) Time-dependent concentration of released AS-IV in the serum of the treatment groups AS-IV and AS-IV@HdECM (n = 3). (D,E) Bar graphs depicting CK-MB and cTnI levels in each group (n = 5). (F) Representative echocardiographic images of different groups at 14 and 28 days post the treatment. Assessment of cardiac function parameters: (G) Left ventricular ejection fraction (LVEF), (H) Left ventricular fractional shortening (LVFS), (I) left ventricular internal diameter at end-systole (LVIDs), and (J) left ventricular internal diameter at end-diastole (LVIDd) (n = 5). All bar graphs include individual data points.

Article Snippet: On days 1, 3, and 7 post-injection, the retention of the compounds in the pericardial cavity was monitored using a small animal in vivo fluorescence imaging system (PerkinElmer IVIS Spectrum).

Techniques: In Vivo, Fluorescence, Injection, Concentration Assay

Brain homing ability, sequential targeting capability, and cytotoxicity assessment. (a) Illustration of Ang-Lip@BAY/GW1929 sequentially transported across the BBB, followed by targeting microglia. (b) Schematic of the BBB transwell model. (c) In vitro uptake by BV-2 cells of RhB-labeled Lip@BAY/GW1929 and Ang-Lip@BAY/GW1929 by fluorescent imaging (scale bar = 50 μm). (d, e f, and g) Fluorescent staining of (CD86 (d) and CD206 (f)), and quantification analysis ((e) and (g)) of the different conditions-treated BV-2 cells in an BBB model in vitro . (h) In vivo imaging of Cy5.5-labeled Ang-Lip@BAY/GW1929 in normoxia mice and CIH-induced mice. (i) Quantitative assessment of in vivo fluorescence intensity of brain at different time intervals under the Cy5.5 channel (n = 3). (j, k) In vitro cytotoxicity assay of Lip (j) and Ang-Lip@BAY/GW1929 (k) at different concentrations against BV-2 cells for 24 h. (l) Cytotoxicity of BV-2 cells treated with various samples. (m) CLSM images of BV-2 cells stained with calcein-AM (green, viable) and PI (red, dead) treated with Lip (G1), Lip@BAY (G2), Lip@GW1929 (G3), Lip@BAY/GW1929 (G4), and Ang-Lip@BAY/GW1929 (G5). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Journal: Materials Today Bio

Article Title: Intelligent nanoliposome ameliorate chronic intermittent hypoxia-mediated neuronal injury via a dual regulation microglial inflammation strategy

doi: 10.1016/j.mtbio.2026.102865

Figure Lengend Snippet: Brain homing ability, sequential targeting capability, and cytotoxicity assessment. (a) Illustration of Ang-Lip@BAY/GW1929 sequentially transported across the BBB, followed by targeting microglia. (b) Schematic of the BBB transwell model. (c) In vitro uptake by BV-2 cells of RhB-labeled Lip@BAY/GW1929 and Ang-Lip@BAY/GW1929 by fluorescent imaging (scale bar = 50 μm). (d, e f, and g) Fluorescent staining of (CD86 (d) and CD206 (f)), and quantification analysis ((e) and (g)) of the different conditions-treated BV-2 cells in an BBB model in vitro . (h) In vivo imaging of Cy5.5-labeled Ang-Lip@BAY/GW1929 in normoxia mice and CIH-induced mice. (i) Quantitative assessment of in vivo fluorescence intensity of brain at different time intervals under the Cy5.5 channel (n = 3). (j, k) In vitro cytotoxicity assay of Lip (j) and Ang-Lip@BAY/GW1929 (k) at different concentrations against BV-2 cells for 24 h. (l) Cytotoxicity of BV-2 cells treated with various samples. (m) CLSM images of BV-2 cells stained with calcein-AM (green, viable) and PI (red, dead) treated with Lip (G1), Lip@BAY (G2), Lip@GW1929 (G3), Lip@BAY/GW1929 (G4), and Ang-Lip@BAY/GW1929 (G5). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The CIH-bearing mice and normoxia-treated mice (n = 3) were respectively fixed in the mouse tail vein injection holder and injected intravenously with Cy5.5-marked Ang-Lip@BAY/GW1929 (100 μg/mL, 100 μL) using a 1 mL syringe, and then monitored the fluorescence changes in the mouse brain during the specified time period (0.5, 2, 4, and 8 h) using in vivo fluorescence imaging (PerkinElmer IVIS Spectrum in vivo imaging system) after intraperitoneal anesthesia and quantified assessment.

Techniques: In Vitro, Labeling, Imaging, Staining, In Vivo Imaging, In Vivo, Fluorescence, Cytotoxicity Assay