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目的探讨他汀类药物保护高糖诱导的糖尿病肾小球损伤的可能机制。方法给予25 mmol/L葡萄糖刺激的同时给予不同浓度的氟伐他汀处理分化后的足细胞36 h。采用蛋白免疫印迹法检测α平滑肌肌动蛋白(α-SMA)、纤维粘连蛋白(FN)、CD2相关蛋白(CD2AP)和Wilms肿瘤1基因(WT-1)蛋白的表达;间接免疫荧光法检测αSMA。结果低糖(5.6 mmol/L)条件下小鼠足细胞表达高水平的WT-1、CD2AP,基本不表达αSMA和FN;予25 mmol/L葡萄糖作用36 h后,足细胞中αSMA和FN表达水平升高,同时WT-1和CD2AP表达水平降低。在高糖条件下给予不同浓度的氟伐他汀处理,结果表明氟伐他汀可部分逆转高糖的上述作用,且存在一定的剂量依赖性。结论氟伐他汀可在一定程度上抑制高糖诱导的足细胞发生向间叶细胞表型的转分化。
Objective To investigate the possible mechanism of statins for protecting diabetic glomerular injury induced by high glucose. Methods Differentiated podocytes were treated with different concentrations of fluvastatin for 36 h after stimulation with 25 mmol / L glucose. The expressions of α-SMA, FN, CD2AP and WT-1 were detected by Western blotting. The expression of αSMA was detected by indirect immunofluorescence assay. . Results The podocytes expressing high level of WT-1 and CD2AP in the low glucose (5.6 mmol / L) group did not express αSMA and FN. After treated with 25 mmol / L glucose for 36 h, the expressions of αSMA and FN in podocytes Increased, while WT-1 and CD2AP expression levels decreased. Fluvastatin at different concentrations was administered under high glucose conditions. Fluvastatin could partially reverse the above effects of high glucose, and there was a dose-dependent manner. Conclusion Fluvastatin can inhibit the transdifferentiation of podocyte phenotype induced by high glucose to a certain extent.