【摘要】目的 观察吡格列酮(PIO)对脂多糖(LPS)作用下大鼠腹膜间皮细胞(RPMC)细胞增殖、凋亡及其肿瘤坏死因子α(TNF-α)表达的影响。 方法 胰蛋白酶-EDTA消化法原代培养RPMC；并用MTT,流式细胞仪和ELISA法来分析吡格列酮对LPS影响下RPMC增殖、凋亡及其分泌TNF-α的影响。 结果 LPS能显著抑制RPMC的增殖(P＜0．01)，促进RPMC的凋亡(P＜0．01)，而5～20靘ol/L的吡格列酮能部分逆转LPS对RPMC增殖的抑制作用(P＜0．01)，抑制LPS所致的RPMC的凋亡(P＜0．01)；LPS能显著增加RPMC表达TNF-α，而5～20靘ol/L的吡格列酮能减弱LPS上调RPMC表达TNF-α的作用(P＜0．01)。 结论 吡格列酮可能通过逆转LPS对RPMC的增殖抑制作用，抑制LPS所致的RPMC的凋亡,减弱 LPS上调RPMC表达炎症因子TNF-α的作用，进而促进RPMC的增殖修复,控制腹膜炎症，为改善间皮细胞损伤和防治腹膜透析相关腹膜炎提供实验依据。

【Abstract】 Objective To observe the effect of pioglitazone on cell proliferation, apoptosis and tumor necrosis factor-α (TNF-α) expression in rat peritoneal mesothelial cell (RPMC) stimulated with lipopolysaccharide (LPS). Methodology RPMCs were isolated after enzymatic digestion, cultured, and identified by phase contrast inverted microscope and immunocytochemistry method. MTT method was used to observe the effects of lipopolysaccharide (10ng/ml) and pioglitazone (5, 10, and 20μmol/L) on cell proliferation. Apoptosis rate was determined by flow cytometry, and TNF-α in culture medium was assayed by ELISA. Results LPS inhibited cell proliferation significantly (P＜0.01), and induced apoptosis (P＜0.01) and TNF-α expression (P＜0.01) in RPMC. These changes could be partially reversed by 5～20μmol/L pioglitazone (P＜0.01). Conclusion Pioglitazone reverses the inhibition of cell proliferation, the increase of apoptosis rate, and the higher expression of fibrosis cytokine TNF-α in RPMCs induced by LPS, through which peritoneal damage is repaired and the inflammation is improved. Therefore, our experimental evidences suggest the prevention and treatment approaches for peritoneal mesothelial cell injury and dialysis-related peritonitis.