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尾加压素Ⅱ及其受体在大鼠肾成纤维细胞中的表达及银杏叶的干预作用

王 丹1,2,李 才1,李相军1,石 艳1,苗春生1   

  1. (1.吉林大学药学院实验药理与毒理学教研室,吉林 长春130021;2.北华大学基础医学院病理学教研室,吉林 吉林132001)
  • 收稿日期:2008-04-21 修回日期:1900-01-01 出版日期:2008-11-28 发布日期:2008-11-28
  • 通讯作者: 李 才

Expression of urotensinⅡand its receptor GPR14 in renal interstitial fibroblasts and intervention of ginkgo bioba extract

WANG Dan1,2,LI Cai1,LI Xiang-jun1,SHI Yan1,MIAO Chun-sheng1   

  1. (1.Department of Experimental Pharmacology and Toxicology,School of Pharmacy,Jilin University,Changchun 130021,China; 2. Department of Pathology,School of Basic Medical Sciences,Beihua University,Jilin 132001,China)
  • Received:2008-04-21 Revised:1900-01-01 Online:2008-11-28 Published:2008-11-28
  • Contact: LI Cai

摘要: 目的:探讨血管紧张素Ⅱ(AngⅡ)对大鼠肾间质成纤维细胞尾加压素Ⅱ(UⅡ)及其受体(GPR14)表达的影响和银杏叶(GBE)的干预作用。方法:体外培养大鼠肾成纤维细胞,以未处理细胞作为正常对照组,以AngⅡ作为刺激因素,分别加入终浓度为0、25、50、100和200 g•L-1的GBE,RT-PCR检测各组细胞UⅡ及GPR14 mRNA表达,免疫印迹法检测各组细胞UⅡ及GPR14蛋白含量,ELISA法检测培养上清中Ⅰ型胶原(ColⅠ)含量。结果: AngⅡ组UⅡ、GPR14表达量及培养上清中ColⅠ含量明显高于正常对照组(P<0.01),与AngⅡ刺激组比较,AngⅡ+GBE组UⅡ及GPR14的mRNA表达量下降(P<0.01),蛋白含量减少(P<0.01或P<0.05),培养上清中ColⅠ含量明显降低(P<0.01或P<0.05)。结论:GBE可抑制AngⅡ诱导的肾间质成纤维细胞UⅡ及受体mRNA表达,降低其蛋白含量,减少细胞外基质ColⅠ分泌。

关键词: GPR14, 血管紧张素Ⅱ, 成纤维细胞

Abstract: Abstract:Objective To explore the effects of angiotensinⅡ products on urotensinⅡ(UⅡ) and its receptor GPR14 expression in cultured renal interstitial fibroblasts and the intervention of ginkgo bioba extract(GBE). Methods The rat renal fibroblasts were cultivated in vitro,untreated cells were acted as normal control group,AngⅡ as the stimulating factor,the cells were treated with GBE with concentrations of 0,25,50,100 and 200 g•L-1,the mRNA and protein levels of UⅡ and GPR14 were measured by RT-PCR and Western blotting,the content of collagenⅠ in supernatant was detected by ELISA method. Results Compared with AngⅡ group,the mRNA and protein levels of UⅡ and GPR14 were significantly down-regulated (P<0.01 or P<0.05),the contents of ColⅠ in supernatant were markedly decreasedin AngⅡ+GBE group(P<0.01 or P<0.05). Conclusion GBE  can down regulate the UⅡ and GPR14 mRNA expression,decrease the protein levels of UⅡ and GPR14,and reduce the ColⅠ secretion in cultured fibroblasts.

Key words: GPR14, angiotensinⅡ, fibroblasts

中图分类号: 

  • R692.32