1,25(OH)_2D_3对血管紧张素Ⅱ诱导的肾小管上皮细胞转化的抑制作用  

Inhibition of 1,25(OH)_2D_3 on transformation of renal tubular epithelial cells induced by angiotensin Ⅱ

作　　者：康红[1] 曹琳[2] 喻洁[2] 欧阳琳娜[2] 陈姗[2] 郑维[2] 

机构地区：[1]湖南省人民医院急诊科,湖南长沙410005 [2]湖南省人民医院普外科,湖南长沙410005

出　　处：《中国现代医学杂志》2014年第10期1-5,共5页China Journal of Modern Medicine

基　　金：国家自然科学基金(No:20972046)

摘　　要：目的探讨1,25(OH)2D3对血管紧张素Ⅱ(AngⅡ)诱导的肾小管上皮细胞转化起始过程的抑制作用,为临床肾间质纤维化的防治提供理论依据。方法分离SD大鼠肾小管上皮细胞,将其分为对照组、AngⅡ诱导组(AngⅡ终浓度10-8mol/L)以及AngⅡ(10-8mol/L)+1,25(OH)2D3干预组[1,25(OH)2D3终浓度分别为10-6mol/L、10-7mol/L、10-8mol/L],培养48 h后收集各组细胞。利用酶联免疫吸附实验检测ColⅠ和FN;Real-time RT-PCR检测肾小管上皮细胞TGF-β1mRNA表达;Western Blot检测肾小管上皮细胞TGF-β1蛋白表达。结果实验48 h后,AngⅡ组TGF-β1mRNA表达、蛋白表达及培养上清中ColⅠ和FN浓度均较对照组显著增高,AngⅡ+10-6mol/L1,25(OH)2D3组TGF-β1mRNA表达、蛋白表达较对照组明显增高,但细胞培养上清中ColⅠ和FN浓度仅略有增高,差异无显著性,随着1,25(OH)2D3浓度的降低(10-7mol/L,10-8mol/L),TGF-β1mRNA表达、蛋白表达,细胞培养上清中ColⅠ和FN浓度也随之显著增高(P<0.05)。结论 1,25(OH)2VD3可以部分抑制AngⅡ诱导的肾小管上皮细胞EMT,其机制可能是通过抑制肾小管上皮细胞TGF-β1基因与蛋白表达、减少肾小管上皮细胞ColⅠ和FN分泌实现的。To investigate inhibition of 1,25（OH）2D3on initial process of renal tubular epithelial cells transformation induced by angiotensin II, and provide a theoretical basis for prevention and treatment of clinical renal interstitial fibrosis. 【Methods】Renal tubular epithelial cells of SD rats were isolated and divided into control group, the experimental group induced by Ang Ⅱ（10-8 mol/L of final concentration）, and the intervention groups induced by Ang Ⅱ（10-8 mol/L） ＋1,25（OH）2D3（10-6mol/L, 10-7mol/L, 10-8mol/L of final concentrations）, the cells were collected after 48 hours. Col Ⅰ and FN were detected using the enzyme-linked immunosorbent assay; TGF-β1mRNA expression of renal tubular epithelial cells were detected by real-time RT-PCR; Western Blotting detectedTGF-β1protein expression of tubular epithelial cells. 【Results】Experiment after 48 hours, TGF-β1mRNA, protein expressions of tubular epithelial cells and Col I, FN concentrations of cell culture supernatant were significantly higher in Ang Ⅱ group than the control group, TGF-β1mRNA and protein expressions of AngⅡ＋10-6 mol/L of 1,25（OH）2D3 group were significantly higher than the control group, but Col Ⅰ and FN concentrations of the cell culture supernatant were only slightly higher, the difference were not significant. With 1,25（OH）2D3concentration decreased, TGF-β1mRNA and protein expressions of tubular epithelial cells, Col Ⅰ and FN concentrations of cell culture supernatant also were significantly higher. 【Conclusion】1,25（OH）2D3can be partially inhibited EMT on Ang Ⅱ-induced renal tubular epithelial cells. The mechanism may be achieved through inhibition of renal tubular epithelial cells on TGF-β1 gene and protein expressions, and decreasing Col Ⅰ and FN secretion from renal tubular epithelial cells.

关 键 词：肾小管上皮细胞 1 25(OH)2D3 血管紧张素Ⅱ 转化生长因子 大鼠 

分 类 号：R-332[医药卫生]