Emodin suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose
Emodin suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose
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大黄素通过p38MAPK通路抑制高糖培养的大鼠系膜细胞增殖和纤连蛋白表达
DOI：
10.1016/j.mce.2009.03.006
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发表时间：
2009-08-13
影响因子：
4.1
通讯作者：
Huang, Heqing
中科院分区：
文献类型：
--
作者：
Li, Xuejuan;Liu, Weihua;Huang, Heqing
我们的前期研究表明大黄素可以改善糖尿病肾病大鼠的肾功能，但其分子机制尚不清楚。本研究观察大黄素对高糖诱导的大鼠肾小球系膜细胞增殖及纤维连接蛋白（FN）表达的影响，并探讨其可能的作用机制。MTT法检测细胞增殖活性，流式细胞仪检测细胞周期。Western blot检测系膜细胞FN、p-p38 MAPK、t-p38 MAPK、p-CREB、PPAR γ和CTGF蛋白表达水平。我们的研究结果表明，大黄素显着抑制HG诱导的细胞增殖和逮捕细胞周期的进展。大黄素处理后，FN、磷酸化p38 MAPK、磷酸化CREB和CTGF蛋白表达明显降低，而PPAR γ蛋白水平明显升高。结论：大黄素通过抑制CREB、PPAP γ和CTGF参与的p38 MAPK通路抑制HG诱导的大鼠系膜细胞增殖和FN表达，提示大黄素在糖尿病肾病治疗中具有潜在作用。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
Our previous findings demonstrated that emodin could improve the renal function in rats with diabetic nephropathy, but little is known about its molecular mechanisms. In this study, we investigated the effects of emodin on high glucose (HG)-induced cell proliferation and fibronectin (FN) protein expression in rat mesangial cells, and explored the possible mechanism. Cell proliferation and cell cycle were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assay, respectively. The protein levels of FN, p-p38MAPK, t-p38MAPK, p-CREB, PPAR gamma, and CTGF in rat mesangial cells were detected by Western blot. Our results demonstrated that emodin significantly suppressed HG-induced cell proliferation and arrested cell cycle progress. Protein expression of FN, phospho-p38MAPK, phospho-CREB and CTGF was markedly reduced, and PPAR gamma protein level was significantly increased after emodin treatment. In conclusion, emodin suppressed HG-induced cell proliferation and FN expression in rat mesangial cells through inhibiting the p38MAPK pathway involved CREB, PPAP gamma and CTGF, suggesting a potential role of emodin in the treatment of diabetic nephropathy. (C) 2009 Elsevier Ireland Ltd. All rights reserved.