Effect of ginkgolide B on hepatic ischemia-reperfusion injury in mice with fatty liver disease and its mechanism

Objective To investigate the effect of ginkgolide B on hepatic ischemia-reperfusion injury in mice with fatty liver disease and its mechanism. Methods A total of 25 male C57BL/6J mice were fed with 60% high-fat diet for 16 weeks, and then they were divided into sham-operation group (laparotomy and suture), model group (occlusion of blood flow in the middle and left lobes of the liver for 1 h, followed by reperfusion for 6 h), ginkgolide B group (intraperitoneal injection of 25 mg/kg ginkgolide B twice, followed by the treatment in the model group), GW9662 group (intraperitoneal injection of 1 mg/kg GW9662 twice, followed by the treatment in the model group), and GW9662+ginkgolide B group (intraperitoneal injection of 25 mg/kg ginkgolide B+1 mg/kg GW9662 twice, followed by the treatment in the model group). At 6 h after administration and surgery, the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured for each group; Western blotting was used to measure the protein expression levels of Bax, Bcl-2, and PPARγ in liver tissue; oil red O staining was used to measure the degree of fatty changes in the liver, and HE staining was used to measure the degree of necrosis in liver tissue. Results Oil red O staining showed that the degree of fatty changes in the liver had reached the level of fatty liver disease in each group. The se-rum enzymatic analysis showed that the ginkgolide B group and the GW9662+ginkgolide B group had significantly lower serum le-vels of ALT and AST than the model group (P<0.05), and the ginkgolide B group had a significantly lower serum level of ALT than the GW9662+ginkgolide B group (P<0.05). HE staining showed that the ginkgolide B group had a significantly lower percentage of necrotic area in liver tissue than the model group and the GW9662+ginkgolide B group (P<0.05). Western blotting showed that the ginkgolide B group had a significantly lower expression level of Bax in liver tissue than the model group (P<0.05), as well as significantly higher expression levels of Bcl-2 and PPARγ than the model group and the GW9662+ginkgolide B group (P<0.05). Conclusion Ginkgolide B can alleviate ischemia-reperfusion injury in mice with fatty liver disease by upregulating PPARγ in liver tissue.