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过氧化物酶体增殖物激活受体γ对TNFα诱导的肾脏内髓集合管上皮细胞损伤的保护作用
林沁,顾勇,林善锬,LINQin,GUYong,LINShan-yan
0
()
摘要:
目的:观察过氧化物酶体增殖物激活受体(PPAR)γ高表达对小鼠肾脏内髓集合管上皮细胞(IMCD)炎性刺激的反应.方法:实验分为4组:IMCD空白对照组,IMCD+TNFα刺激组,转染PPARγ野生型质粒的转染空白组(PPARγ-IMCD组)和PPARγ-IMCD+TNFα刺激组.TNFα刺激:采用TNFα 50 ng/ml作用24 h;质粒转染:将小鼠野生型PPARγ1质粒转染于IMCD细胞使PPARγ高表达.ELISA方法检测细胞上清液MCP-1、TGFβ1分泌量.结果:转染PPARγ野生型质粒的IMCD细胞PPARγ mRNA和蛋白高表达.1MCD空白对照组和PPARγ-IMCD转染空白组相比,细胞上清液MCP-1和TGFβ1含量无显著性差异;IMCD+TNFα刺激组培养上清液中MCP-1和TGF-β1表达明显增加(与IMCD空白对照组相比,P<0.005),PPARγ-IMCD+TNFα刺激组培养上清液中MCP-1和TGFβ1的分泌与IMCD+TNFα刺激组相比显著减少(P<0.05和P<0.005).结论:IMCD细胞转染PPARγ野生型质粒使得PPARγ高表达后具有抗炎和抗纤维化作用.
关键词:  过氧化物酶体增殖物激活受体γ、肿瘤坏死因子α、肾小管上皮细胞
DOI:10.3724/SP.J.1008.2006.00599
投稿时间:2005-12-29修订日期:2006-04-18
基金项目:国家自然科学基金(300200125);霍英东基金(81038);上海市卫生局科委基金(03JC14084).
Protective effect of peroxisome proliferator-activated receptor γ on TNFα-induced injury of inner medullary collecting duct cells
林沁,顾勇,林善锬,LIN Qin,GU Yong,LIN Shan-yan
()
Abstract:
Objective:To observe the protective effect of peroxisome proliferator-activated receptor γ (PPARγ) on TNFα- induced injury of the inner medullary collecting duct (IMCD) cells. Methods: Cultured IMCD cells were randomly divided into blank control, TNFα stimulation, PPARγ transfection (pPPARγ-control) and PPARγ transfection + TNFα stimulation groups. Stimulation was induced with 50 ng/ml TNFα for 24 h and mouse wild-type PPARγ plasmid was used to transfect IMCD cells. Cell supernatant MCP-1 or TGFβ1 was detected by ELISA method. Results: IMCD cells transfected with wild-type PPARγ plasmid had high expression of PPARγ mRNA and protein. The contents of MCP-1 and TGFβ1 in the supernatant were similar in blank control group and pPPARγ-control group. Compared with blank control group, TNFα stimulation group had decreased contents of MCP-1 and TGFβ1 in the supernatant (P〈0. 005), but the contents of TNFα stimulation group were significantly higher than those of PPARγ transfection + TNFα stimulation group (P〈0.05 and P(0. 005, respectively). Conclusion: IMCD cells over expressing PPARγ have anti-inflammatory and anti-fibrosis effects.
Key words:  peroxisome proliferator-activated receptor γ  tumor necrosis factor-α  inner medullary collecting duct cells