Fig 2: Effects of bovine lactoferrin (BL) on inflammatory factors and expression of colonic mucosa-related defense proteins in dextran sulfate sodium salt (DSS) mice. (A–E) ELISA of inflammatory factors, IL-1β, IL-6, IL-10, TGF-α, and TNF-β of colon tissue in mice. (F) Immunofluorescence results and analysis of MUC2. (G) Immunofluorescence results and analysis of Reg3γ. (H) Immunofluorescence results and analysis of HBD-2. (I) Immunofluorescence results and analysis of cAMP. One-way ANOVA was used to compare the three groups. *P < 0.05 vs. control; #P < 0.05 vs. DSS.

Fig 3: IR-61 suppresses chronic inflammation in vivo.a–c Relative mRNA levels of the inflammatory cytokines in the epi WAT (a) and liver (b), plasma concentrations of cytokines (c) of NCD-fed and HFD-fed mice treated preventatively with IR-61 or the vehicle control. d–f Relative mRNA levels of the inflammatory cytokines in epi WAT (d) and liver (e), plasma concentrations of the cytokines (f) of the mice with established obesity treated with IR-61 or vehicle control. g Representative images of H&E stained sections of VAT from NCD-fed or HFD-fed mice treated preventatively with IR-61 or vehicle control (Scale bars, 100 µm). White arrows show crown-like structures. h, i Adipocyte size distribution (left panel) and the average size of adipocytes (right panel) were assessed on H&E-stained slices in (g). j Relative mRNA levels of the macrophage marker in the epi WAT of NCD-fed and HFD-fed mice treated with IR-61 or vehicle control. k Relative mRNA levels of the inflammatory cytokines in epi WAT of the mice with established obesity treated with vehicle, IR-61, BMS-303141, and BMS-303141+IR-61. Sample sizes are (a) n = 5/5/5/5 mice, (b) Tnf n = 4/4/3/4 mice, Il6 n = 3/4/4/5 mice, Il1b n = 3/4/4/3 mice, (c) n = 3/3 mice, (d) n = 5/5 mice, (e) Tnf n = 4/5 mice, Il6 n = 5/4 mice, Il1b n = 4/5 mice, (f) Tnf n = 4/4 mice, IL-6 n = 4/4 mice, IL-1ß n = 5/5 mice, (g-i) n = 6/6/7/6 mice, (j) n = 5/5/5/5 mice, (k) Tnf n = 5/5/4/4 mice, Il6 n = 4/5/5/4 mice, Il1b n = 4/5/5/5 mice. Data are presented as the mean ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001; two-sided Student’s t-test). Exact p-values are given in the Source Data file. Source data are provided as a Source Data file.

Fig 4: Comprehensive analysis of granulosa cell subpopulations and inflammatory changes in the PCOS Environment(A) UMAP plot delineating distinct GC subpopulations.(B) Changes in the proportions of GC subpopulations in PCOS compared to control.(C) Heatmap illustrating the top 5 markers defining each GC subset.(D) Visualization of GC subpopulations in the control group and PCOS group via distinct UMAP clusters.(E and F) GO enrichment analysis and KEGG pathway enrichment analysis for the top 50 specific genes in GC5.(G) IL-17 and TNF-α in the ovarian homogenate of the control group and PCOS mice (n = 9).(H) Western blot detection for IL-17 and TNF-α protein levels in control and DHEA-treated GC (n = 3).(I) qRT-PCR detection for Il17a and Tnf mRNA expression in control and DHEA-treated GC (n = 3). Data are represented as mean ± SD, ∗p < 0.05 by t-test.

Fig 5: The mechanism of how ADSCs-Exo prevents the onset of MRONJ. Zol promotes macrophage M1 polarization and pyroptosis, causing the release of IL-1β. IL-1β can stimulate the IL-1R on the cell surface to form a positive feedback effect, cascading pyroptosis and inflammatory response. Excessive pyroptosis and the release of inflammatory factors delay the healing of tooth extraction sockets. IL-1RA derived from ADSCs-Exo can competitively bind to the IL-1R on the cell membrane surface and block the effect of IL-1β. IL-1RA inhibits the macrophage M1 polarization and pyroptosis by inhibiting the NF-κB/NLRP3/IL-1β axis, reducing the release of proinflammatory cytokines such as IL-1β and TNF-a in the tooth extraction sockets, thus promoting wound healing and preventing the occurrence of MRONJ.