PPARγ活化对TGF-β1诱导肾小管上皮细胞趋化因子表达的干预作用

目的：观察PPARγ活化对转化生长因子-β1（TGF-β1）诱导的肾小管上皮细胞炎症相关趋化因子表达的影响,探讨其在肾脏纤维化中的干预作用。方法：体外培养肾小管上皮细胞HK-2,LDH法检测15d-PGJ2和TGL对HK-2的细胞毒性,应用不同浓度的15d-PGJ2和TGL作用于TGF-β1诱导下的HK-2细胞,应用实时荧光定量PCR技术和ELISA方法检测趋化因子单核细胞趋化蛋白-1（MCP-1）、白细胞介素-8（IL-8）表达的变化。结果：5μmol/L15d-PGJ2和2.5μmol/LTGL不影响HK-2细胞MCP-1和IL-8mRNA基础表达和蛋白分泌。TGF-β1作用24h时,2.5μmol/L和5μmol/L15d-PGJ2及2.5μmol/LTGL均能有效干预TGF-β1诱导的MCP-1mRNA表达和蛋白的分泌（P〈0.05）。IL-8的表达与MCP-1相似,2.5μmol/L和5μmol/L15d-PGJ2能显著抑制TGF-β1诱导的IL-8表达,TGF-β1诱导24h时2.5μmol/LTGL能显著抑制IL-8mRNA表达（P〈0.05）。结论：PPARγ激动剂15d-PGJ2和TGL作用均能有效干预TGF-β1诱导的肾小管上皮细胞趋化因子MCP-1和IL-8的表达,可能具有有效干预肾间质炎症作用。

Inhibitory Effects of Activated PPARγ on TGF-β1 Induced Chemotatic Factors Expression in Renal Tubular Epithelial Cells

Objective：To investigate the effect of PPARγ on the expression of chemotatic factors in cultured renal tubular epithelial cells induced by TGF-β1,and to study the inhibitory effects of PPARγ agonists in the process of renal fibrosis.Methods：Cultured human renal tubular epithelial cells（HK-2） were stimulated by TGF-β1 and pretreated of 15 d-PGJ2 and TGL.The cytotoxicity was tested by LDH method.The expression of chemotatic factors,such as monocyte chemoattractant protein-1（MCP-1） and interleukin-8（IL-8） were measured by Real-time fluorescent Quantitative PCR analyses and ELISA.Results：5 μmol/L 15 d-PGJ2 and 2.5 μmol/L TGL could not influence the basal MCP-1 and IL-8 mRNA expression and protein excretion in HK-2 cells.After being stimulated by TGF-β1 for 24 hours,Both 2.5 μmol/L、5 μmol/L 15 d-PGJ2 and 2.5 μmol/L TGL had inhibitory effects on the expression of MCP-1 mRNA and protein.Both 2.5 μmol/L and 5 μmol/L 15 d-PGJ2 also had such effect on the expression of IL-8,while TGL just had such effect on the 24th hour.Conclusion：PPARγ agonists 15 d-PGJ2 and TGL could effectively inhibit renal interstitial inflammation and TGF-β1-induced expression of chemotatic factors MCP-1 and IL-8 in the cultured HK-2 cells.