吡格列酮对小鼠肾小管上皮细胞炎症性刺激的保护作用

Protective effect of Pioglitazone on TNFα-mediated IMCD cell injury

目的观察吡格列酮对小鼠肾脏内髓集合管上皮细胞（IMCD）炎性刺激是否具有保护作用。方法培养成片的IM-CD细胞随机分为6组：空白对照组,PIO对照组,GW9662对照组,TNFα刺激组,PIO＋TNFα组,GW9662＋PIO＋TNFα组。MTT方法观察TNFα刺激下细胞增殖情况,ELISA方法检测细胞培养上清液中MCP-1和TGF-β1含量。结果TNFα50ng/ml刺激使IM-CD细胞增殖抑制（P〈0.05）,细胞培养上清液中MCP-1和TGF-β1含量明显增加（P〈0.05）。Pio能阻断TNFα刺激所致的IM-CD细胞增生抑制,减少细胞分泌MCP-1和TGF-β1。而上述保护性作用可被PPARγ特异性拮抗剂GW9662所阻断。结论Pio能保护IMCD细胞免受TNFα刺激所致的损伤,其保护性作用可能通过PPARγ途径发挥效应。

Objective To observe the protective effect of pioglitazone on TNFα mediated IMCD celt （ mouse inner medullar collecting duct cell） injury. Methods Cultured IMCD cells were random divided into vehicle control group, PIO control group, GW9662 control group, TNFα stimulated group, PIO ＋ TNFα group and GW9662 ＋ PIO ＋ TNFαgroup. Cell proliferation response to TNFα were evaluated by MTF assay. Cell supernatant MCP-1 and TGF-β1content were detected by ELISA. Results TNFα （50ng/ml） stimulating strikingly caused cell proliferation arrest （ P 〈 0.05 ） and markedly increased MCP-1 and TGF-β1 content in cell supernatant （ P 〈 0.05 ）. Pioglitazone treatment prevented TNFα-induced IMCD proliferation arrest （ P 〈 0. 05 ）, inhibited TNFα-mediated MCP-1 and TGF-β1 secretion. PPAR3, specific antagonist GW9662 can block the protective effect of pioglitazone. Conclusion PIO has anti-inflammation protective role in TNFα-me- diated IMCD cell injury, and the mechanism is supposed to be through the PPAR-y pathway.