芪蓟肾康方对AngⅡ所致大鼠肾小球系膜细胞增殖变化中JNK-AP1影响

目的：探讨芪蓟肾康方通过JNK信号通路对大鼠肾小球系膜细胞的影响。方法：体外培养大鼠肾小球系膜细胞，用血管紧张素Ⅱ刺激系膜细胞增生，给予芪蓟肾康方黄酮干预，用酶联免疫吸附（ELISA）法检测肾小球系膜细胞上清液 c-Jun 氨基末端激酶（JNK）、活化蛋白1（AP-1）、纤维粘连蛋白（FN）蛋白表达；实时定量 PCR 法检测 JNK、AP-1 mRNA 的表达。结果：与正常组比较，模型组及治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN 蛋白表达明显升高（P〈0.05或 P〈0.01）；与模型组比较，治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN 蛋白表达明显降低（P〈0.05或 P〈0.01）。与正常组比较，模型组及治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN mRNA 表达明显升高（P〈0.05或 P〈0.01）；与模型组比较，治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN mRNA明显降低（P〈0.05）。结论：芪蓟肾康方可以通过下调肾小球系膜细胞JNK、AP-1 mRNA及蛋白的表达水平，抑制 JNK 信号转导，降低 AP-1的活性，减少 FN 的增殖，从而减轻 GMC 增生，延缓肾小球的损伤，防止肾小球的硬化。

Effects of Qi-Ji Shen-Kang on JNK-AP1 Signal Pathway among AngⅡ Induced Rats with Glomerular Mesangial Cell Proliferation

This study was aimed to investigate the effects of Qi-Ji Shen-Kang （QJSK） on glomerular mesangial cell （GMC） through the c-Jun N-terminal kinase （JNK） signal pathway. GMC was cultured in vitro and the proliferation was induced with Angiotensin Ⅱ （AngⅡ）. Then, QJSK was used to inhibit the proliferation. ELISA was used in the detection of protein expressions of JNK, activator protein-1 （AP-1） and fibronectin （FN）. Q-PCR was used in the de-tection of expression of JNK and AP-1mRNA. The results showed that compared with the normal group, protein ex-pressions of JNK, AP-1 and FN of GMC among rats in the model group and the treatment group were obviously in-creased （P〈 0.05 or P〈 0.01）. Compared with the model group, protein expressions of JNK, AP-1 and FN of GMC among rats in the treatment group were obviously decreased （P 〈 0.05 or P 〈 0.01）. Compared with the normal group, expressions of JNK, AP-1 and FN mRNA of GMC among rats in the model group and the treatment group were obviously increased （P〈 0.01 or P〈 0.05）. Compared with the model group, expressions of JNK, AP-1 and FN mRNA of GMC among rats in the treatment group were obviously decreased （P〈 0.05）. It was concluded that QJSK can downregulate expressions of JNK and AP-1 mRNA, as well as the protein expressions of JNK, AP1 and FN, in order to inhibit JNK signal pathway, decrease activity of AP-1, reduce FN proliferation. It relieved proliferation of GMC, slowed down glomerulus damnification, and prevented glomerular sclerosis.