Abstract: Objective To explore the effect of galangin (Gal) on inflammation in hepatitis B rats. Methods The rats were randomly divided into control group, hepatitis B group, Gal-L and Gal-H groups, positive drug lamivudine group and Gal-H+AMPK inhibitor (compound C) group with 12 in each. After modeling, medication treatment was performed once a day for 8 weeks. The level of alanine aminotransferase (ALT), total bilirubin (TBIL) and aspartate aminotransferase (AST) in the serum of rats were detected. HE staining microscopy was applied to detect pathological changes in liver tissue. TUNEL staining microscopy was applied to detect cell apoptosis in liver tissue. Chromatin immuno-precipitation was applied to detect HBV viral load in liver tissue. ELISA was applied to detect the levels of monocyte chemotactic protein-1(MCP-1), interleukin-12(IL-12), and tumor necrosis factor-α(TNF-α) in liver tissue. Western blot was applied to detect the expression of caspase-3, Bcl-2 associated X protein (Bax), p-AMPK and SIRT1 proteins in liver tissue. Results Compared with hepatitis B group, the liver damage of rats in the Gal-L group, Gal-H group and lamivudine group was alleviated; The level of serum AST, TBIL, and ALT, apoptosis rate, HBV viral load and the level of MCP-1, IL-12, TNF-α as well as the expression of caspase-3 and Bax proteins in liver tissue were all reduced. The expression of p-AMPK and SIRT1 proteins in liver tissue increased(P＜0.05). Compound C baffled inhibitory effects of high-dose Gal on inflammation, cell apoptosis, and HBV viral load in liver tissue of hepatitis B rats. Conclusions The mechanism of Gal in inhibiting inflammation, cell apoptosis and HBV virus replication in hepatitis B rats is potentially attributed to up-regulation of the AMPK/SIRT1 pathway.

Key words: galangin, adenosine 5'-monophosphate-activated protein kinase/silent information regulator 2 homologue 1 pathway, Hepatitis B, liver injury, inflammation