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目的探讨预处理（preconditioningPc）对大鼠肝脏缺血再灌注（ischemia／reperfusion，I／R）损伤的影响及其机制。方法制备大鼠肝脏原位I／R损伤的模型，采用免疫组织化学技术结合图像分析方法定量检测原癌基因c-fos表达的情况和肝组织脂质过氧化产物丙二醛（MDA）的变化。结果I／R损伤早期可引起损伤区肝细胞核内原癌基因c－fos的大量表达；PC明显减少了c－fos表达的细胞数量以及减轻肝脏脂质过氧化的程度。结论PC对大鼠肝脏I／R损伤有明显的保护作用，可能的机制之一是抑制肝I／R损伤后原癌基因c-fos的表达和灭活自由基减少脂质过氧化物的生成。
Objective To investigate the effect and mechanism of preconditioning PC on hepatic ischemia / reperfusion (I / R) injury in rats. Methods I / R injury model of rat liver was established. The expression of proto-oncogene c-fos and the change of malondialdehyde (MDA) in liver tissue were quantitatively detected by immunohistochemistry and image analysis . Results In the early stage of I / R injury, the expression of proto-oncogene c-fos in the nucleus of injured hepatocytes was significantly increased. PC significantly decreased the number of c-fos-expressing cells and the degree of hepatic lipid peroxidation. Conclusions PC has a significant protective effect on rat liver I / R injury. One of the possible mechanisms is to inhibit the expression of proto-oncogene c-fos after liver I / R injury and to inactivate free radicals to reduce the formation of lipid peroxides .