茶多酚对大鼠肝脏缺血-再灌注损伤的保护作用

目的探讨茶多酚对大鼠肝脏缺血再灌注损伤的保护作用及其机制。方法健康雄性SD大鼠30只，随机均分为4组：假手术正常对照组6只；肝脏缺血再灌注损伤模型组8只；茶多酚低浓度于预组8只（75mg／kg）；茶多酚高浓度于预组8只（150mg／kg）．缺血30min再灌注60min检测肝组织MDA含量、GSH-PX活性及血浆ALT含量。光镜下比较各组肝组织损伤情况。结果肝缺血再灌注模型组ALT、MDA含量明显高于假手术正常对照组（P〈0．01），GSH-PX活力则降低（P〈0．01）；茶多酚低浓度及高浓度组ALT，MDA含量均明显低于肝缺血再灌注模型组（P〈0．01），而GSH-Px活力均高于肝缺血再灌注模型组（P〈0．01）；光镜观察茶多酚低浓度及高浓度预处理组肝细胞损伤明显小于肝缺血再灌注模型组。结论茶多酚对大鼠肝脏缺血再灌注损伤具有显著的保护作用。

The protective effect of teapolyphenols on hepatic ischemia reperfusion injury in rats

Objective To investigate the protective effect and its role of teapolyphenols on hepatic ischemia reperfusion injury in rats.Methods Thirty male Sprague-Dawley rats were randomly divided into four groups: six rats were served as pseudo-operation normal control group, eight rats were served as hepatic ischemia reperfusion injury model group, eight rats were low dose teapolyphenols group(75 mg/kg) , eight rats were served as high dose teapolyphenols group(150 mg/kg). After 30 minutes hepatic ischemia and 60 minutes reperfusion , the MDA level and GSH-PX activity in the liver of each group were detected , and the content of ALT in the serum also were examined . The injury circumstance of the liver tissue in each group were compared by optical microscope.Results The MDA level in the liver and the content of ALT in the serum of hepatic ischemia reperfusion injury model group were evidently higher than those in pseudo-operation normal control group(P<0.01), and the GSH-PX vim in the liver was decreas(P<0.01); Comparing to the hepatic ischemia reperfusion injury model group, the MDA level in the liver and the content of ALT in the serum of low and high dose teapolyphenols group were evidently decreased(P<0.01), while the GSH-PX contents in the liver is increased(P<0.01). The change could be observed by the optical microscope which liver cell injury of the teapolyphenols groups was evidently slight than that of the hepatic ischemia reperfusion injury model group. Conclusion The teapolyphenols have a prominent protective effect on hepatic ischemia reperfusion injury in rats.