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Inhibitory effects of emodin on the proliferation of cultured rat vascular smooth muscle cell‐induced by angiotensin II
Author(s) -
Wang ShiJun,
Liu YunYing,
Fan FangHua,
Yan Jie,
Wang XingXiang,
Chen JunZhu
Publication year - 2008
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2301
Subject(s) - emodin , proliferating cell nuclear antigen , vascular smooth muscle , cell growth , angiotensin ii , immunohistochemistry , aloe emodin , mtt assay , microbiology and biotechnology , staining , cell , biology , chemistry , endocrinology , immunology , biochemistry , smooth muscle , receptor , genetics
Rhubarb, used as a traditional Chinese medicine for centuries, offers therapeutic potential for cardiovascular and other diseases. Emodin, extracted from the root extract of rhubarb has sparked increasing interest for therapeutic application. The main objective was to study the effect of emodin on cultured vascular smooth muscle cells (VSMCs) proliferation induced by angiotensin II (Ang II) and the expression of proto‐oncogene c‐myc. VSMCs were cultured by the explant method, then incubated for 24, 48 and 72 h with emodin (10–80 µ m ) and Ang II, or were left untreated (control). Cell proliferation was measured by MTT assay and immunohistochemical staining for proliferating cell nuclear antigen (PCNA), respectively. The expression of c‐myc was measured by immunohistochemical staining and image analysis technique. Ang II increased the cell proliferation compared with the control group ( p < 0.01). The expression of PCNA and c‐myc was increased compared with the control group ( p < 0.01). After pretreatment with emodin, the above indexes were obviously reduced compared with the Ang II group ( p < 0.01). These findings suggested that emodin inhibited VSMCs proliferation induced by Ang II. Inhibition of the expression of c‐myc might be correlated with the inhibitory effects. Copyright © 2007 John Wiley & Sons, Ltd.