大黄素对高糖培养的GMC增殖、FN表达及p38MAPK的影响

Effects of emodin on cell proliferation,FN expression and p38MAPK pathway in rat mesangial cells cultured under high glucose

目的本研究旨在观察大黄素对高糖培养的大鼠肾小球系膜细胞(GMC)的增殖与细胞外基质的主要成分——纤维连接蛋白(FN)表达的影响,观察大黄素对高糖培养的p38MAPK信号转导通路的影响,以探讨大黄素调节p38MAPK信号通路抗糖尿病肾脏纤维化的分子作用机制。方法 MTT比色法检测细胞活力;流式细胞仪检测细胞周期分布;Western blot方法检测FN、p-p38MAPK蛋白表达情况。结果高糖能够诱导大鼠GMC增殖、上调FN的表达以及促进p38MAPK活化,与正常培养组相比差异有统计学意义(P<0.05);大黄素可以抑制高糖诱导的大鼠GMC增殖、FN表达与p38MAPK活化,与高糖组相比差异有统计学意义(P<0.05)。结论大黄素抗糖尿病肾脏纤维化的作用可能与大黄素抑制p38MAPK信号通路密切相关。

Aim To investigate the effects of emodin on cell proliferation and fibronectin （FN） protein ex-pression in rat mesangial cells cultured under high glu-cose （HG） , and then to explore the role of p38MAPK pathway in the protective effect of emodin on mesangial ceils cultured under HG. Methods Cell proliferation was determined by MTF, cell cycle was determined by flow cytometry, and the protein expression of FN, p-p38MAPK protein in mesangial cells were detected by Western blot. Results HG could induce cell prolifer- ation and enhance expression of FN, phospho-p38MAPK in rat mesangial cells compared with controlgroup （P 〈 0. 05 ）. Emodin could inhibit cell prolifera- tion and expression of FN, phospho-p38MAPK in rat mesangial cells cultured under HG （P 〈 0. 05 ）. Con- clusion In conclusion, emodin suppresses HG-in- dueed cell proliferation and FN expression in rat me-sangial cells through inhibiting the p38MAPK pathway, suggesting a potential role of emodin in the treatment of diabetic nephropathy.