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目的 探讨天冬氨酸特异性半胱氨酸蛋白酶 (Cystene -requiringaspartateprotease ,Caspase)在鼠肝缺血再灌注 (IschemicReperfusion ,IR)损伤中的变化及缺血预处理 (IschemicPreconditioning ,IP)的保护作用机制。方法 3 0只大鼠随机分为IR组、IP组及假手术组 (S)组。检测再灌注术后 3h血清AST、ALT水平、肝组织caspase3活性、肝细胞凋亡指数 (ApoptosisIndex ,AI)和电镜下超微结构改变。结果 ⑴血清AST、ALT改变 :IP组和IR组较S组显著升高 (P <0 0 1) ,其中IR组升高最明显 ,与IP组比较差异有显著性 ( P <0 0 1)。⑵肝组织Caspase3活性 ,IR组和IP组较S组明显升高 ( P <0 0 1) ,IR组最明显 ,与IP组比较差异显著 ( P <0 0 1)。⑶肝细胞AIS组未见明显调亡细胞 ,IR组和IP组AI差异有显著性 (P <0 0 1)。⑷电镜IR组超微结构破坏明显 ,IP组相对较轻 ,S组基本正常。结论 IR损伤可激活Caspase3活性 ,促进肝细胞凋亡 ,从而加重肝脏损害 ,IP可明显减轻肝脏IR损伤 ,可能的机制之一是下调Caspase3的活性来抑制肝细胞调亡。
Objective To investigate the protective effect of Caspase (Caspase) on ischemia-reperfusion injury in rat liver and the protective effect of Ischemic Preconditioning (IP) . Methods 30 rats were randomly divided into IR group, IP group and sham operation group (S). The levels of AST, ALT, activity of caspase 3, apoptosis index (Apoptosis index) and ultrastructure changes in the 3 h after reperfusion were detected. Results (1) Serum AST and ALT changes: IP group and IR group were significantly higher than those of S group (P <0.01), of which IR group had the most obvious increase, compared with IP group (P <0.01) . (2) The activity of Caspase3 in liver tissue was significantly increased in IR group and IP group as compared with S group (P <0.01). The IR group was the most obvious. Compared with IP group, the difference was significant (P <0.01). (3) There was no obvious apoptotic cells in the AIS group of hepatocytes, and there was a significant difference in the AI between IR group and IP group (P <0.01). ⑷ electron microscopy IR group obvious damage to ultrastructure, IP group is relatively light, S group was normal. Conclusion IR injury can activate Caspase3 activity, promote apoptosis of hepatocytes, and thus aggravate liver damage. IP can significantly reduce hepatic IR injury. One of the possible mechanisms is the down-regulation of Caspase3 activity to inhibit hepatocyte apoptosis.