title: Emodin inhibits tumor necrosis factor-α-induced migration and inflammatory             responses in rat aortic smooth muscle cells.
abstract: Emodin, a naturally occurring anthraquinone derivative in oriental herbal             medicine, has been shown to exert a variety of pharmacological activities. The             goal of this study was to determine the effects of emodin on the modulation of             cell proliferation, migration, inflammatory responses, and matrix metalloproteinase             (MMP)-2 and MMP-9 expression in tumor necrosis factor (TNF)-α-induced rat aortic             smooth muscle cells (RASMCs). Cell proliferation and migration were measured using             the MTT assay and the transwell chamber assay, respectively. Quantitative real-time             PCR and western blot analysis were used to detect MMP expression. Gel shift was             used for analysis of nuclear factor (NF)-κB activation. In addition, the expression             of several inflammatory genes was also analyzed. Treatment of RASMCs with emodin             significantly and dose-dependently attenuated TNF-α-induced proliferation, migration,             mRNA and protein expression of MMP-2 and MMP-9, and NF-κB activation. Furthermore,             emodin significantly inhibited TNF-α-evoked inflammatory responses, as demonstrated             by the reduction in the expression of inflammatory genes. These results suggest             that emodin inhibits TNF-α-induced proliferation, migration, MMP-2 and MMP-9 expression             as well as inflammatory responses in cultured RASMCs, supporting the notion that             emodin may have potential application in clinical atherosclerosis disease.
authors.affiliation: Department of Circulation, Fengtian Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning, PR China.
authors.forename: Liang
authors.initials: L
authors.lastname: Meng
authors.forename: Dongming
authors.initials: D
authors.lastname: Yan
authors.forename: Weidong
authors.initials: W
authors.lastname: Xu
authors.forename: Jian
authors.initials: J
authors.lastname: Ma
authors.forename: Bin
authors.initials: B
authors.lastname: Chen
authors.forename: Hong
authors.initials: H
authors.lastname: Feng
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology*; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics; D024202:Electrophoretic Mobility Shift Assay; D004642:Emodin / Q000494:pharmacology*; D007249:Inflammation / Q000473:pathology*; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D020782:Matrix Metalloproteinases / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D018836:Inflammation Mediators; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D020782:Matrix Metalloproteinases; D004642:Emodin