title: Emodin suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose.
abstract: 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, PPARgamma, 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 PPARgamma 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, PPAPgamma and CTGF, suggesting a potential role of emodin in the treatment of diabetic nephropathy.
authors.affiliation: School of Pharmaceutical Sciences, Sun Yat-Sen University, Guagnzhou, Guangdong, China.
authors.forename: Xuejuan
authors.initials: X
authors.lastname: Li
authors.forename: Weihua
authors.initials: W
authors.lastname: Liu
authors.forename: Qin
authors.initials: Q
authors.lastname: Wang
authors.forename: Peiqing
authors.initials: P
authors.lastname: Liu
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Deng
authors.forename: Tian
authors.initials: T
authors.lastname: Lan
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Zhang
authors.forename: Baoming
authors.initials: B
authors.lastname: Qiu
authors.forename: Hairong
authors.initials: H
authors.lastname: Ning
authors.forename: Heqing
authors.initials: H
authors.lastname: Huang
mesh_terms: D000818:Animals; D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D055513:Connective Tissue Growth Factor / Q000378:metabolism; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004642:Emodin / Q000494:pharmacology*; D005353:Fibronectins / Q000378:metabolism*; D005355:Fibrosis; D005947:Glucose / Q000494:pharmacology*; D050527:Mesangial Cells / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D047495:PPAR gamma / Q000378:metabolism; D051381:Rats; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D017362:Cyclic AMP Response Element-Binding Protein; D005353:Fibronectins; D047495:PPAR gamma; D055513:Connective Tissue Growth Factor; D048051:p38 Mitogen-Activated Protein Kinases; D005947:Glucose; D004642:Emodin