Ning Jian-Ping, Yang Shen, Ning Chen, Zeng Ying-Hui, Liu Lun-Zhi, Liu Jun
Department of Nephrology, Xiangya Hospital, Central South University, Changsha 41000, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2007 Feb;32(1):104-8.
To determine the effect of integrin-linked kinase(ILK) in renal tubular epithelial cells and its relation to tubular epithelial-myofibroblast transdifferentiation.
Wistar rats were randomly divided into 3 groups, Group normal control (n=10), Group diabetic without therapy(n=10) and Group diabetic with Losartan 20mg/(kg . d)(n=10). Five rats were killed in each group at the 8th and 16th week. The left kidneys were kept for HE and Masson staining to observe the pathological variations in the renal interstitium. ILK, alpha-SMA and Vimentin in renal tubular epithelial cells were detected by immunohistochemistry analysis.
Compared with the control group, ILK, alpha-SMA and Vimentin in renal tubular epithelial cells in Group diabetes gradually increased in immunohistochemistry (P<0.01); ILK was consistent with the pathological variation of renal interstitium and was positively correlated to alpha-SMA(rs=0.621, P<0.05). In comparison with the Group diabetes, the expression of ILK, alpha-SMA and Vimentin in renal tubular epithelial cells was apparently declined (P<0.01) in Group diabetes with Losartan.
Tubular epithelial myofibroblast transdifferentiation and the over-expression of ILK, between which there may be significant connections, are important events in the progression of diabetic nephropathy. Losartan, a blocker of angiotension II type I receptor, which may down-regulate the expression of ILK in diabetic renal tubular epithelial cells, can restrain the procession of epithelial-myofibroblast transdifferentiation.
探讨整合素连接激酶（ILK）在肾小管上皮细胞中的作用及其与肾小管上皮-肌成纤维细胞转分化的关系。
将Wistar大鼠随机分为3组，正常对照组（n = 10）、糖尿病未治疗组（n = 10）和糖尿病氯沙坦20mg/（kg·d）治疗组（n = 10）。每组分别于第8周和第16周处死5只大鼠，留取左肾行HE和Masson染色，观察肾间质病理变化；采用免疫组化法检测肾小管上皮细胞中ILK、α-SMA和波形蛋白的表达。
免疫组化显示，与对照组相比，糖尿病组肾小管上皮细胞中ILK、α-SMA和波形蛋白表达逐渐增加（P<0.01）；ILK表达与肾间质病理变化一致，且与α-SMA呈正相关（rs = 0.621，P<0.05）。与糖尿病组相比，氯沙坦治疗组肾小管上皮细胞中ILK、α-SMA和波形蛋白表达明显下降（P<0.01）。
肾小管上皮-肌成纤维细胞转分化及ILK过表达是糖尿病肾病进展中的重要事件，二者可能密切相关。血管紧张素Ⅱ1型受体阻滞剂氯沙坦可下调糖尿病肾小管上皮细胞中ILK的表达，抑制上皮-肌成纤维细胞转分化进程。
