Anemoside B4 ameliorates TNBS-induced colitis through S100A9/MAPK/NF-κB signaling pathway

Abstract Background Despite the increased morbidity of ulcerative colitis (UC) in developing countries, available treatments remain unsatisfactory. Therefore, it is urgent to discover more effective therapeutic strategies. Pulsatilla chinensis was widely used for treatment inflamed intestinal diseases including UC thousands years China. Anemoside B4, most abundant triterpenoid saponin isolated from P. , exerts anti-inflammatory and antioxidant effects may be active compounds, which responsible effects. However, mechanism how anemoside B4 executes its biological functions still elusive. Methods Here, we 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced rat model evaluate effect B4. Blood samples rats were collected hematology analysis. The inflammation-associated factors investigated by enzyme-linked immunosorbent assay (ELISA). Cell proliferation apoptosis determined with EdU cell TUNEL assay. proteins regulated identified label-free quantitative proteomics. significantly down-regulated verified Western blotting mRNA expression analyzed real-time RT-PCR. Results results showed that ameliorated TNBS-induced symptoms, tissue damage, inflammatory infiltration, pro-inflammatory cytokine production, slowed colon. Quantitative proteomic analyses discovered 56 altered rats. These mainly clustered tricarboxylic (TCA) cycle respiratory electron transport chain. Among proteins, S100A9 one associated NF-κB MAPK signaling pathways pathogenesis UC. Further experiments revealed suppressed downstream genes TLR4 In vitro, could inhibit pathway induced recombinant protein human epithelial Caco-2 cells. Moreover, inhibits neutrophils recruitment activation colon TNBS. Conclusions Our demonstrate prevents inhibiting through deactivating S100A9, suggesting a promising candidate colitis.