The protective effect of gastrodin on the hepatic ischemia-reperfusion injury in mice / 中华肝胆外科杂志

ABSTRACT

Objective To investigate the protective effect of gastrodin (Gas) on the hepatic ischemia-reperfusion injury (HIRI) in mice,and study possible mechanisms.Methods Forty male C57BL/6 mice were randomly divided into sham-operated group (Sham),HIRI group,gastrodin-treated groups with low and high does (Gas-L,Gas-H,respectively),and cobalt protoporphyrin(CoPP) group(n =8).Mice in Gas-L,Gas-H,and CoPP groups were injected intraperitoneally with individual drugs and dose before operation.Except for Sham group,an 70％ volume HIRI model was established by means of 60 minutes ischemia and then 6 hours reperfusion in the other groups.The levels of serum AST and ALT in each group were compared.The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver tissue were measured;The level of TNF-αt,IL-6,IL-10 and heme oxygenase-I (HO-1) mRNA level were detected by real time quantitative PCR.Liver tissue was stained with H&E.The hepatocyte apoptosis was studied by TUNEL.Results Respectively,the serum ALT level in the HIRI,Gas-L,Gas-H and CoPP groups was (5 057.34±290.80)U/L,(3 917.49±198.10) U/L,(3 645.63± 171.10) U/L,(2 977.78± 179.00) U/L,and the ALT level was (5 871.25 ± 819.01) U/L,(4 660.88 ± 505.96) U/L,(4 182.00 ± 507.51) U/L,(3 788.65±462.14)U/L.The serum level of ALT and AST in Gas-L,Gas-H and CoPP groups was lower than HIRI group (P＜ 0.05).The apoptotic index in Gas-L,Gas-H and CoPP groups respectively was (37.89±4.27)％,(32.59±3.78)％,(20.45-±2.49)％,which was lower than group (58.92±3.32)％ (P＜ 0.05).Compared with HIRI group,the TNF-α and IL-6 mRNA level in Gas-L,Gas-H and CoPP groups were decreased,and the levels of IL-10 and HO-1 mRNA were increased.Simultaneously,the activity of SOD was promoted,whereas the levels of MDA was reduced (P＜0.05).Conclusions Gastrodin shows an protective function aganist liver ischemia-reperfusion injury in mice by inhibiting inflammation,oxidative stress and cell apoptosis.The up-regulation of HO-1 by gastrodin may be the possible mechanism.