维生素E在大鼠肝脏缺血再灌注损伤中的作用

目的探讨维生素E在肝组织缺血再灌注(I/R)损伤的保护机制及对缺血预处理(IP)的影响。方法采用大鼠原位半肝缺血再灌注和缺血预处理模型,缺血前通过灌胃给予维生素E(250mg/kg),分析血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)、全血还原型谷胱甘肽(GSH)、肝组织脂质过氧化物(LPO)、超氧化物歧化酶(SOD)含量及肝组织病理改变等各项指标。结果I/R导致明显的肝损伤,IP减轻肝I/R损伤,维生素E能减轻肝组织缺血再灌注损伤,但可以部分抵消IP的保护作用。结论维生素E能减轻肝组织缺血再灌注损伤,其作用是通过减少氧自由基产生而实现的。IP对鼠肝I/R有明显的保护作用,IP期间产生的一定量的自由基,对随后的I/R的保护作用具有重要意义。维生素E导致氧自由基减少是肝IP保护作用的不利因素。

The role of vitamin E in rat hepatic ischemia/reperfusion injury

Objective To investigate the protective mechanism of vitamin E in rat hepatic ischemia/reperfusion injury and how vitamin E relates to hepatic ischemia preconditioning (IP). Methods Rat models of in-situ hemi-hepatic I/R injury and IP were given intragastic vitamin E (250 mg/kg) before ischemia. Serum activities of GPT, GOT, LDH, vitamin E, whole blood levels of GSH, LPO, vitamin E and SOD as well as changes in liver pathology were determined and analyzed. Results IP significantly attenuated the severity of I/R-induced hepatic injury. Vitamin E also showed similar protective effect, however, pre-IP administration of vitamin E partly counteracted the IP protective effects. Conclusion Vitamin E significantly attenuated hepatic ischemia/reperfusion injury, possibly by reduction of oxygen free radicals. A quantity of oxygen free radicals generated during IP may significantly underlie the subsequent protection from I/R injury. Vitamin E induced reduction of oxygen free radicals may be a disadvantage against IP hepatoprotection.