基础医学与临床 ›› 2012, Vol. 32 ›› Issue (9): 1088-1092.

• 研究论文 • 上一篇    下一篇

福辛普利抑制LPS诱导的人肾小管上皮HK-2细胞TAK1表达

黄文辉,卢守燕,汤羽   

  1. 甘肃省人民医院
  • 收稿日期:2011-08-29 修回日期:2011-12-25 出版日期:2012-09-05 发布日期:2012-08-28
  • 通讯作者: 卢守燕 E-mail:lsylushouyan@163.com

Fosinopril Suppresses the expression of TAK1 of the Human Renal Tubular Epithelial Cells Induced by LPS

  • Received:2011-08-29 Revised:2011-12-25 Online:2012-09-05 Published:2012-08-28

摘要: 摘要:目的 探讨福辛普利(FOS)对脂多糖(LPS)诱导的人肾小管上皮细胞(HK-2)增殖及对转化生长因子β激活激酶(TAK1)表达的影响。方法 体外培养正常HK-2细胞,分为3组:对照组(Ctrl)、LPS诱导组(10μg/L)、FOS干预组(LPS 10 μg/L+ FOS 1×106 mol/L)。细胞培养12、24和48h,以甲基噻唑基四唑(MTT)法检测细胞增殖情况,酶联免疫吸附(ELISA)法观察细胞上清纤维粘连蛋白(FN)变化,Western-blotting法检测TAK1、FN蛋白表达,实时荧光定量PCR检测TAK1 mRNA的含量。结果 LPS诱导组较对照组细胞的增殖水平[在48小时分别为(0.462±0.013)及( 0.363±0.014) ]、细胞胞浆中FN的含量均显著增高,且自12h开始TAK1蛋白[在48小时分别为(1.627±0.101)及(0.547±0.010) ]及mRNA表达水平上调(P<0.01,P<0.05),FOS干预组细胞增殖[在48小时为(0.396±0.011)]、FN的含量及TAK1的表达[在48小时蛋白表达为(1.308±0.097)]较同时间点LPS组[在48小时蛋白表达为(1.627±0.101)]显著下调(P<0.01)。结论 FOS可能通过抑制HK-2的增生与活化,减轻细胞外基质FN的沉积,起到延缓肾间质纤维化的作用。

关键词: 福辛普利, 人肾小管上皮细胞, 转化生长因子β激活激酶, 肾间质纤维化

Abstract: Abstract:Objective To investigate the effects of fosinopril(FOS) on expression of TAK1 and proliferation of the human renal tubular epithelial cells induced by LPS. Methods Human renal tubular epithelial (HK-2) cells were divided into three groups: blank control group(Ctol), LPS group (10 μg/L), FOS group (LPS 10 μg/L+ FOS 1×106 mol/L). At 12, 24, 48 hours, HK-2 proliferation was detected by methyl thiazolyl tetrazolium (MTT) assay. The change of fibronectin (FN) in the supernatants of the cultured HK-2 was detected by enzymelinked immunosorbent assay (ELISA). The protein expressions of TAK1 and FN were measured by Western blot. The mRNA expressions of TAK1 was measured by real-time quantitative PCR. Results The cell proliferation and the expression of FN were increased, and the expressions of protein and mRNA of TAK1 in LPS group were upregulating significantly compared with control group from 12 h (P<0.01,P<0.05), but they were downregulating in FOS group compared with LPS group(P<0.01). Conclusion FOS probably delay renal interstitial fibrosis by inhibiting proliferation and activation of HK-2 and decreasing accumulation of extracellular matrix.

Key words: Fosinopril, Human renal tubular epithelial cells, TGFβ-activated kinase 1, Renal interstitial fibrosis