〔Abstract〕 Objective To investigate the protective effect and mechanisms of silent information regulator 1(SIRT1) agonist resveratrol on monocrotaline-induced Hepatic sinusoidal obstruction syndrome(HSOS) in rats. Methods Thirty-two male Sprauge-Dawley(SD) rats were randomly divided into three group, with 8 rats in the control group and 12 rats in each of the monocrotaline group and resveratrol group. The monocrotaline group and resveratrol group were given monocrotaline(160 mg/kg) by single gavage. The resveratrol group was intraperitoneally injected with resveratrol solution [30 mg/(kg·d)] one day before intragastric administration. The experiment was terminated 2 days after the monocrotaline administration. Serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), total bilirubin(TBiL), glutathione(GSH) and malondialdehyde(MDA) in liver homogenate were detected. The pathological change of liver tissue was observed. The protein expression levels of SIRT1, hypoxia-inducible factor-1α(HIF-1α), and vascular endothelial growth factor(VEGF) in liver were detected by Westernblot. Results Compared with the control group, the serum ALT, AST and TBiL in monocrotaline group increased(allP<0.01), GSH in liver homogenate decreased(P<0.01), MDA increased(P<0.01). Disordered arrangement, degeneration and necrosis of liver cells, congestion and dilation of hepatic sinuses and damage of central vein endothelium were observed. SIRT1 decreased(P<0.01), HIF-1α and VEGF protein expression increased(allP<0.01). After resveratrol treatment, serum ALT, AST and TBiL obviously decreased(P<0.05;P<0.05;P<0.01). GSH in liver homogenate increased(P<0.01), MDA decreased(P<0.01). And resveratrol also could inhibit the liver pathological damage caused by monocrotaline. SIRT1 protein expression increased(P<0.01), HIF-1α and VEGF protein expression also decreased(allP<0.01). Conclusion Resveratrol can improve Hepatic sinusoidal obstruction syndrome caused by monocrotaline in rats, and the mechanism is related to its activation of SIRT1, inhibition of HIF-1α/VEGF signaling pathway and antioxidanion.