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

Protective effect of peroxisome proliferator-activated receptor γ on TNFα-induced injury of inner medullary collecting duct cells

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(PPAR-γIMCD组)和PPARγ-IMCD+TNFα刺激组。TNFα刺激:采用TNFα50 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PPARγmRNA和蛋白高表达。IMCD空白对照组和PPAR-γIMCD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),PPAR-γIMCD+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。

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.