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objectivesTo investigate the protective effect of

methodsSD rats were randomized into sham-operated group, BDL model group, low- and high-dose HXQJL treatment groups, Ex527 (a Sirt1 inhibitor) group (EX527), and HXQJL+Ex527 group. Liver histopathological changes and collagen deposition were observed using HE and Sirius Red staining, and serum levels of ALT, AST, ALP, and GGT of the rats were measured using biochemical assays. The expression levels of α‑SMA, FN, COL I, Atg5, Beclin1, p62, LC3B, and Sirt1 were determined by RT-PCR and Western blotting. Immunofluorescence staining was used to detect the expression of α-SMA, LC3B, and Sirt1.

resultsCompared with the sham-operated rats, the rats in BDL model group exhibited increased hepatocyte injury, inflammatory cell infiltration, and collagen deposition area with elevated serum levels of ALT, AST, ALP, and GGT, enhanced haptic expressions of α‑SMA, FN, COL I, Atg5, and Beclin1, an increased LC3B-II/I ratio, and lowered hepatic expressions of p62 and Sirt1. All these changes were significantly alleviated in the two HXQJL treatment groups but aggravated in EX527 treatment group. Compared with those in high-dose HXQJL group, the protective effects of HXQJL on liver tissue injury, liver function, liver fibrosis, and autophagy were obviously mitigated by treatment with Ex527.

conclusionsHXQJL has protective effect against BDL-induced liver fibrosis in rats by modulating the Sirt1-autophagy signaling pathway.