摘要Objective:To explore the effect and mechanism of Dahuang Zhechong Pill(DHZCP)on liver fibrosis.Methods:Liver fibrosis cell model was induced by transforming growth factor-β(TGF-β)in hepatic stellate cells(HSC-T6).DHZCP medicated serum(DMS)was prepared in rats.HSC-T6 cells were divided into the control(15％normal blank serum culture),TGF-β(15％normal blank serum+5 ng/mL TGF-β),DHZCP(15％DMS+5 ng/mL TGF-β),DHZCP+PDTC[15％DMS+4 mmol/L ammonium pyrrolidine dithiocarbamate(PDTC)+5 ng/mL TGF-β],and PDTC groups(4 mmol/L PDTC+5 ng/mL TGF-β).Cell activity was detected by cell counting kit 8 and levels of tumor necrosis factor-α(TNF-α),interleukin(IL)-1 β,IL-6,aspartate aminotransferase(AST)and alanine aminotransferase(ALT)in the cell supernatant were determined by enzyme-linked immunosorbnent assay.Western blot was used to measure the expressions of p38 mitogen-activated protein kinase/nuclear factor kappa B/transforming growth factor-β1(p38 MAPK/NF-κ B/TGF-β 1)pathway related proteins,and the localization and expressions of these proteins were observed by immunofluorescence staining.Results:DHZCP improved the viability of cells damaged by TGF-β and reduced inflammatory cytokines and ALT and AST levels in the supernatant of HSC-T6 cells induced with TGF-β(P＜0.05 or P＜0.01).Compared with the TGF-β group,NF-κ B p65 levels in the DHZCP group were decreased(P＜0.05).p38 MAPK and NF-κ B p65 levels in the DHZCP+PDTC were also reduced(P＜0.01).Compared with the TGF-β group,the protein expression of Smad2 showed a downward trend in the DHZCP,DHZCP+PDTC,and PDTC groups(all P＜0.01),and the decreasing trend of Samd3 was statistically significant only in DHZCP+PDTC group(P＜0.01),whereas Smad7 was increased(P＜0.05 or P＜0.01).Conclusion:DHZCP can inhibit the process of HSC-T6 cell fibrosis by down-regulating the expression of p38 MAPK/NF-κ B/TGF-β 1 pathway.