锌对肝缺血再灌注损伤的对抗作用及其机制研究

目的:观察外源性锌对缺血再灌注肝脏(HIR)的防护作用并探讨其机制,包括对粘附分子表达的影响。方法:复制大鼠HIRI模型,灌胃给锌,观察实验动物肝组织形态、血清转氨酶活性、血清丙二醛(MDA)含量及粘附分子表达的改变。结果:在肝脏缺血30min,再灌注90min时,大鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)活性增高,肝细胞结构受损,血清MDA含量升高,肝组织中细胞间粘附分子-1(ICAM-1)和血管细胞粘附分子-1(VCAM-1)两种粘附分子表达增强;锌+缺血再灌注组大鼠血清GPT、GOT活性及血清MDA含量均明显低于缺血再灌注组,肝组织粘附分子表达亦较弱,肝细胞的结构基本正常。结论:外源给锌可以明显减轻肝脏缺血再灌注损伤,抗脂质过氧化和抑制粘附分子表达是其作用的重要机制。

The antagonistic effect of zinc on hepatic ischemia-reperfusion injury and the mechanism

AIM:To investigate the antagonistic effect of zinc on hepatic ischemia- reperfusion (HIR) injury and the effect of zinc on the expression of adhesion molecules in rat liver to clarify the mechanisms involved. METHODS:After zinc supplementation (5 μmol/kg bw,po), the changes in hepatocellular morphology,ALT and AST activities in serum,MDA levels in serum,and expression of ICAM-1,VCAM-1 in liver of the animals subjected to HIR were examined.RESULTS:The results showed that HIR (30 minutes of ischemia followed by 90 minutes of reperfusion) significantly increased ALT, AST activities and MDA levels in serum. The destruction of hepatic structure was observed in HIR rats. In the mean time, the expression of adhesion molecule was enhanced.After zinc administration, ALT and AST activities in serum and MDA levels in serum were all decreased. The structure of hepatocyte was nearly normal.The further experiment showed that adhesion molecule expression was suppressed.CONCLUSION:These results indicate that zinc may protect liver against ischemia-reperfusion injury by inhibiting the production of free radicals and the expression of adhesion molecule.