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目的观察瑞芬太尼预处理和缺血预处理对大鼠肝脏缺血再灌注损伤早期细胞凋亡的影响及其机制。方法SD大鼠72只,随机分为假手术组(S组),缺血再灌注组(IR组),瑞芬太尼预处理组(R组),缺血预处理组(IP组)。分别在再灌注1、3、5h处死6只大鼠,取左肝内叶组织免疫组织化学法分别测定各组Bcl-2和Bax的表达,原位细胞凋亡法测定肝细胞凋亡的情况,光镜、电镜观察肝脏组织病理变化。结果与S组相比,IR组细胞凋亡指数、Bax表达均增高(P<0.05),而瑞芬太尼预处理和缺血预处理组减弱了缺血再灌注上述指标的升高(P<0.05),二者没有区别;IR组Bcl-2表达减少(P<0.05),瑞芬太尼预处理和缺血再灌注组可增强其在肝组织的表达(P<0.05),二者没有区别。病理检查显示瑞芬太尼预处理和缺血预处理减轻肝缺血再灌注损伤。结论瑞芬太尼预处理及缺血预处理都有抑制大鼠肝脏缺血再灌注损伤早期细胞凋亡的作用,均与上调Bcl-2蛋白表达、下调Bax蛋白表达有关,瑞芬太尼可模拟缺血预处理的抗细胞凋亡作用。
Objective To observe the effect and mechanism of remifentanil preconditioning and ischemic preconditioning on hepatic ischemia-reperfusion injury in early stage of apoptosis in rats. Methods Seventy two SD rats were randomly divided into sham operation group (S group), ischemia reperfusion group (IR group), remifentanil pretreatment group (R group) and ischemic preconditioning group (IP group). Six rats were sacrificed at 1,3,5h after reperfusion, respectively. The expression of Bcl-2 and Bax in each group was determined by immunohistochemistry and the apoptosis of hepatocytes was measured by in situ cell apoptosis Light microscope and electron microscope were used to observe the histopathological changes of liver tissue. Results Compared with S group, apoptosis index and Bax expression in IR group were increased (P <0.05), and remifentanil preconditioning and ischemic preconditioning group weakened the above indexes (P <0.05). There was no difference between the two groups. The expression of Bcl-2 in IR group was decreased (P <0.05), and remifentanil preconditioning and ischemia / reperfusion group could enhance the expression of Bcl- no difference. Pathological examination showed that remifentanil pretreatment and ischemic preconditioning alleviated hepatic ischemia-reperfusion injury. Conclusion Both remifentanil preconditioning and preconditioning of ischemic preconditioning can inhibit the apoptosis of liver cells in early stage of ischemia-reperfusion injury in rats. Both of them are related to the up-regulation of Bcl-2 protein expression and down-regulation of Bax protein expression, To simulate the anti-apoptotic effect of ischemic preconditioning.