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Journal: Bioactive Materials
Article Title: Injection site dictates the immune response to a biodegradable polymer and corresponding collagen regeneration
doi: 10.1016/j.bioactmat.2026.04.004
Figure Lengend Snippet: Denser ID tissue architecture leads to greater DAMPs release upon T-gel injection and enhanced macrophage recruitment to the implantation site. (A) Schematic diagram depicting the proposed mechanism: cell damage caused by T-gel injection releases DAMPs (e.g., HMGB1, HSP70, dsDNA and histone DNA), which activate resident macrophages via the DAMPs–TLRs–MyD88–NF-κB signaling axis, promoting secretion of chemokines such as C-C motif chemokine ligands (CCLs) and recruiting additional macrophages/monocytes from local and distal tissues to the injection site. TLRs, Toll-like receptors; MyD88, Myeloid differentiation primary response protein 88; NF-κB, Nuclear factor kappa-light-chain-enhancer of activated B cells. (B) Comparison of maximum pushing force (N) required for ID vs. SC T-gel injection ( n = 3, data represent mean ± s.d.). ∗∗∗∗P < 0.0001. (C) Immunofluorescence analysis of HMGB1 localization and HSP70 expression in tissues one day after ID or SC T-gel injection ( n = 3, data represent mean ± s.d.). ∗∗P < 0.01. (D) Immunofluorescence staining showing nuclear translocation of NF-κB p65 in macrophages (CD68 + cells) one day after ID or SC T-gel injection ( n = 3, data represent mean ± s.d.). ∗∗P < 0.01. (E) RNA-seq analysis of macrophage-related chemokine expression in tissues after ID or SC T-gel injection. “SC ctrl” and “ID ctrl” denote subcutaneous and intradermal injection of normal saline, respectively. Heatmaps show expression levels (FPKM) for each sample. CCL1 and CCL6 did not show significant differences between any groups and are therefore not displayed. (F) Immunofluorescence quantification of CD68 + cells in tissues 7 days after ID or SC T-gel injection ( n = 3, data represent mean ± s.d.). ∗P < 0.05. (G) GO functional analysis of macrophage-associated terms from RNA-seq data after ID or SC T-gel injection.
Article Snippet: After antigen retrieval and blocking, sections were incubated overnight at 4 °C with primary antibodies targeting vimentin, CD68 (ABclonal, A20803), CD31 (R&D SYSTEMS, AF3628), HMGB1 (Cell Signaling Technology, 3935), HSP70 (ABclonal, A23457),
Techniques: Injection, Comparison, Immunofluorescence, Expressing, Staining, Translocation Assay, RNA Sequencing, Saline, Functional Assay
Journal: International Journal of Molecular Sciences
Article Title: Colocasia esculenta Corm Extract Attenuates Ethanol-Induced Gastric Ulcer by Suppressing NF-κB Expression: An Integrated Network Pharmacology Approach and In Vivo Validation
doi: 10.3390/ijms27177693
Figure Lengend Snippet: ( a ) Representative Western blot of NF-κB p65 expression. Representative Western blot bands showing the expression of NF-κB p65 protein in gastric tissues from the different experimental groups following ethanol-induced gastric injury; ( b ) Quantification of NF-κB p65 protein expression. β-Actin was used as the internal loading control. Note: 1, Normal; 2, Negative; 3, Sucralfate; 4, Quercetin; 5, EECE 200 mg/kg; 6, EECE 400 mg/kg; 7, EECE 800 mg/kg.
Article Snippet: Membranes were incubated overnight at 4 °C with primary
Techniques: Western Blot, Expressing, Control
Journal: Frontiers in Microbiology
Article Title: Spermidine protects against ETEC-induced intestinal injury by reshaping the gut microbiota and activating the AhR/IL-22 axis
doi: 10.3389/fmicb.2026.1907051
Figure Lengend Snippet: Spermidine suppresses activation of the TLR4/MyD88/NF-κB signaling pathway in ETEC-infected mice. (A) Representative Western blot images showing the protein expression of TLR4, MyD88, phosphorylated NF-κB p65 (p-p65), total NF-κB p65 (p65), and GAPDH in jejunal tissues. (B–D) Densitometric analyses of TLR4 (B) , MyD88 (C) , and p-p65 (D) protein expression normalized to the corresponding loading controls. Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s multiple-comparison test. ** p < 0.01, *** p < 0.001.
Article Snippet: The primary antibodies used for Western blot were TLR4 (Proteintech, Cat No. 66350-1-Ig, 1:4,000), MyD88 (ABclonal, Cat No. A0980, 1:2,000), p-p65 (ABclonal, Cat No. AP1294, 1:2,000),
Techniques: Activation Assay, Infection, Western Blot, Expressing, Comparison
Journal: Frontiers in Microbiology
Article Title: Spermidine protects against ETEC-induced intestinal injury by reshaping the gut microbiota and activating the AhR/IL-22 axis
doi: 10.3389/fmicb.2026.1907051
Figure Lengend Snippet: Spermidine preserves intestinal barrier integrity in ETEC-infected mice. (A) Representative Western blot images showing the protein expression of ZO-1, occludin, and GAPDH in jejunal tissues. (B–C) Densitometric analyses of ZO-1 (B) and occludin (C) protein expression. (D–F) Serum levels of fluorescein isothiocyanate-dextran 4 kDa (FD4) (D) , diamine oxidase (DAO) activity (E) , and D-lactate (F) as indicators of intestinal permeability and barrier function. Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s multiple-comparison test. ** p < 0.01, *** p < 0.001.
Article Snippet: The primary antibodies used for Western blot were TLR4 (Proteintech, Cat No. 66350-1-Ig, 1:4,000), MyD88 (ABclonal, Cat No. A0980, 1:2,000), p-p65 (ABclonal, Cat No. AP1294, 1:2,000),
Techniques: Infection, Western Blot, Expressing, Activity Assay, Permeability, Comparison
Journal: Frontiers in Microbiology
Article Title: Spermidine protects against ETEC-induced intestinal injury by reshaping the gut microbiota and activating the AhR/IL-22 axis
doi: 10.3389/fmicb.2026.1907051
Figure Lengend Snippet: Pharmacological inhibition of AhR abolishes the protective effects of spermidine against ETEC-induced intestinal injury in vivo . (A) Schematic illustration of the experimental design for AhR inhibition using CH-223191 in the ETEC infection model. (B) Survival curves of mice during the experimental period. (C) Changes in body weight following ETEC challenge. (D) Diarrhea scores. (E) Representative hematoxylin and eosin (H&E)-stained sections of the jejunum. Upper panels show low-magnification views (scale bar = 500 μm), and lower panels show corresponding higher-magnification images of the boxed regions (scale bar = 200 μm). (F) Histopathological injury scores. (G) Quantification of the villus-to-crypt (V/C) ratio. (H–K) Serum concentrations of IL-6 (H) , IL-1β (I) , TNF-α (J) , and IL-10 (K) determined by ELISA. (L–N) Assessment of intestinal permeability by serum FITC-dextran 4 kDa (FD4) (L) , diamine oxidase (DAO) activity (M) , and D-lactate (N) . (O) Representative Western blot images showing the expression of AhR, CYP1A1, ZO-1, and occludin in jejunal tissues. (P–S) Densitometric quantification of AhR (P) , CYP1A1 (Q) , ZO-1 (R) , and occludin (S) protein expression normalized to GAPDH. (T) Serum IL-22 levels measured by ELISA. Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s multiple comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, not significant.
Article Snippet: The primary antibodies used for Western blot were TLR4 (Proteintech, Cat No. 66350-1-Ig, 1:4,000), MyD88 (ABclonal, Cat No. A0980, 1:2,000), p-p65 (ABclonal, Cat No. AP1294, 1:2,000),
Techniques: Inhibition, In Vivo, Infection, Staining, Enzyme-linked Immunosorbent Assay, Permeability, Activity Assay, Western Blot, Expressing