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目的观察缺血预处理对大鼠肝缺血再灌注损伤复灌早期细胞增殖与Cyclin D1表达的影响,探讨缺血预处理保护作用的机制。方法54只SD大鼠随机分成缺血再灌注组(IR)、缺血预处理组(IP)和假手术组(SO),利用肝原位部分缺血再灌注模型,于复灌后0、1、2、4 h取材,应用流式细胞仪,检测各组肝细胞Ki67抗原表达,同时应用Western blot法检测各组蛋白表达的变化。结果与IR组相比,在复灌后0、1 h,IP组肝细胞Ki67表达率明显增高[(28．86±6．34)％比(19．40±5．35)％,(46．82±9．80)％比(22．40±5．08)％,P＜0．05],同时可见IR组复灌后2h Cy- clinD1蛋白始有表达,而IP组在复灌开始时即有表达。结论缺血预处理可促进肝细胞在缺血再灌注损伤后早期细胞增殖与Cyclin D1的表达,可能是其对缺血再灌注损伤起到保护作用的机制之一。
Objective To observe the effect of ischemic preconditioning on cell proliferation and expression of Cyclin D1 at the early stage of reperfusion injury induced by hepatic ischemia-reperfusion in rats and to explore the protective mechanism of ischemic preconditioning. Methods Fifty-four SD rats were randomly divided into three groups: ischemia reperfusion (IR) group, ischemia preconditioning group (IP) and sham operation group (SO) The expression of Ki67 antigen in hepatocytes of each group was detected by flow cytometry at 1, 2 and 4 h. The protein expression of each group was detected by Western blot. Results Compared with IR group, the expression of Ki67 in IP group was significantly increased at 0 and 1 h after reperfusion [(28.86 ± 6.34)% vs (19.40 ± 5.35)%, (46 .82 ± 9.80)% (22.40 ± 5.08)%, P <0.05]. At the same time, the expression of Cy-clinD1 protein was observed 2 hours after reperfusion in IR group, When expressed. Conclusion Ischemic preconditioning can promote the proliferation and expression of Cyclin D1 in hepatocytes at early stage after ischemia-reperfusion injury, which may be one of the protective mechanisms of ischemic preconditioning against ischemia-reperfusion injury.