Fig 2: Effects of BBR on pro-inflammatory cytokines of serum in mice (n = 8). A: CXCL9 content in the serum of each group mice; B: CXCL1 content in the serum of each group mice; C: IL-17 content in the serum of each group mice; D: TNF-acontent in serum of each group mice. N.S: None statistically significant; ##P < 0.01 versus control group; **P < 0.01 versus UC group. &&P < 0.01 versus mesalazine group. BBR_Low: BBR with low dose; BBR_High: BBR with high dose.

Fig 3: Proinflammatory responses prior to pro-fibrotic alterations. (a,c) Cecum lesions were sampled from each experimental group (3–5 mice/group) at the indicated time points post operation, followed by qRT-PCR assessment of expression of proinflammatory cytokine and pro-fibrotic molecule genes (a) and by immunostaining of phosphorylated transcription factors with ImageJ analysis data (c,d) Ifng, interferon ?; Il6, interleukin-6; Tnf, tumor necrosis factor-a; Pai1, plasminogen activator inhibitor type 1; Col1a1, collagen 1a1; Tgfb1, tumor growth factor- ß1. (b) Peritoneal fluid and serum were sampled from human patients at the indicated time points following the beginning of laparotomy, and IL-6 levels were measured using ELISA. Representative photos are shown. Data at 0 day or hour postoperation indicated those in untreated control mice. Data are shown as mean ± SD. *p < 0.05 (Dunnett’s test). Daggers indicate serosa; open brackets indicate adhesion lesions. All experiments were independently repeated twice.

Fig 4: Ingredients-Targets Molecular Docking (A). The binding energy of the main active components of SGFD and the key targets. (B). The binding site of the main active components of SGFD and the key targets. The molecular docking poses of Quercetin—TNF (a), Formononetin—TNF (b), Licochalcone A—IL1ß (c), Kaempferol—TNF (d), Licochalcone A—TNF (e), Isorhamnetin—TNF (f), Quercetin—IL1ß (g), Isorhamnetin—IL1ß (h), Formononetin—PTGS2 (i), Naringenin—TNF (j), Kaempferol—IL1ß (k), Formononetin—IL1ß (l), Naringenin—IL1ß(m), Kaempferol—PTGS2 (n), Isorhamnetin—PTGS2 (o), Kaempferol—MAPK3 (p), Formononetin—MAPK3 (q), Quercetin—PTGS2 (r), Naringenin—IL6 (s), Quercetin—IL6 (t), Licochalcone A—PTGS2 (u), Kaempferol—IL6 (v), Isorhamnetin—IL6 (w), Naringenin—PTGS2 (x), Formononetin—IL6 (y), Naringenin—TP53 (z), Isorhamnetin—MAPK3 (aa), Licochalcone A—MAPK3 (ab), Quercetin—MAPK3 (ac), Licochalcone A—IL6 (ad), Naringenin—MAPK3 (ae), Formononetin—TP53 (af), Licochalcone A—TP53 (ag), Kaempferol—TP53 (ah), Quercetin—TP53 (ai), Isorhamnetin—TP53 (aj).

Fig 5: PUFA ?-3 alleviates sodium nitrite exposure-induced cerebral cortical tissue damage in fetal rats via the NRF1/HMOX1 pathway.(A) TNF and IL-1B concentrations were detected by ELISA, n = 3 rats/group. (B-C) The mRNA and protein expression levels of Tnf, Nos2, and Il1b were detected by qRT-PCR and western blot, n = 3 rats/group. Original blots are presented in S2A Fig. (D) Expression levels of SOX2, ENO2, and TUBB3 in the brain cortical tissue of each group were detected by IF, n = 3 rats/group. (E) IOD data statistics of SOX2, ENO2, and TUBB3 expression in the brain cortical tissue of each group were analyzed by Image-Pro-Plus, n = 3 rats/group. (F-H) Nrf1 and Hmox1 mRNA and protein expression levels were analyzed by qRT-PCR and western blot, n = 3 rats/group. Original blots are presented in S2B Fig. *P < 0.05. IF, immunofluorescence; IL-1B, interleukin-1 beta; IOD, integrated optical density; qRT-PCR, quantitative real-time PCR; TNF, tumor necrosis factor.