大鼠肝脏缺血再灌注损伤c-fos表达及预处理的保护作用

Expression of c-fos following ischemia/reperfusion injury and preconditioning protection in rat liver

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 expression of the immediate early gene c-fos following ischemia/reperfusion injury and the effect of preconditioning on I/R injury in the rat liver. Methods On the role of in situ hepatic I/R injury of the rats, changes of expression of c-fos, which has been hypothesized to be tile key factor in determining tissue regeneration following I/R injury, were examined in the rat liver by immunocy-tochemical technique combined with image analysis method, MDA activity in liver tissues were observed. Results Hepatic I/R injury induced c-fos expression within damaged regions of the rat liver at early phase(1-3h) post reper fusion; PC inhibited c-fos expression and attenuated formation of MDA(P<0.01). Conclusion Our results suggest that PC can protect liver from I/R injury; one of the POSSible mechanisms is to inhibit c-fos expression, inactivate oxygen, free radicals and reduce formation of MDA. [