目的探讨JNK/ATF-2信号通路在。肾脏缺血再灌注损伤(IR)中的作用。方法将60只雄性Wistar大鼠随机分为假手术组(对照组)和缺血再灌注组(IR组),每组30只。IR组制备IR模型。各组分别于再灌注0、10、30min及1、24h各处死6只大鼠,取其肾组织,采用免疫组化及RT—PCR法检测不同时间点肾小管上皮细胞JNK、ATF-2磷酸化蛋白及mRNA表达水平。结果IR组JNK、ATF-2mRNA及蛋白表达早期即有增加,再灌注30min出现高峰,再灌注1h表达略减弱,24h仍有高表达,与假手术组比较,差异均有统计学意义。结论肾脏缺血再灌注后JNK/ATF-2信号通路在肾小管上皮细胞表达明显上调,抑制其表达可减轻肾脏损伤。
Objective To investigate the expression of c-Jun amino-terminal kinase (JNK)/ATF-2 signaling pathway on renal ischemia reperfusion injury in rat. Methods A total of 60 male Wistar rats were randomly divided into sham group (sham group, n = 30) and ischemia-reperfusion group (IR group, n = 30). Rats were sacrificed at different times (0 min, 10 min, 30 min, 1 h, 24 h) after reperfusion. Expression of JNK, ATF-2 were analyzed by methods of immuno- histochemistry and RT-PCR. Results In IR group, the expression of JNK, ATF-2 increased at early time, peaked at 30 min, and last for 24 h. Compared with sham group, the differences were significant. Conclusion JNK/ATF-2 signaling pathway can be activated in renal tubular epithelial cells after renal ischemia reperfusion.