期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 307, 期 1-2, 页码 157-162出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2009.03.006
关键词
Emodin; Mesangial cells; p38MAPK; PPAR gamma; CTGF
资金
- National Natural Science Foundation of China [30873427]
- Science and Technology Program of Guangdong province, PR China [2008B030301117]
- Guangdong/Hong Kong Critical Technology Field [2008A030600008]
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.
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