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AE treatment (5, 10, and 20 \u00b5M) of preadipocyte cells resulted in a significant (<jats:italic>p<\/jats:italic>&lt; 0.05) decrease in glycerol phosphate dehydrogenase and triglyceride levels as well as an increase in lactate dehydrogenase activity and attenuated lipid accumulation compared with untreated differentiated adipocytes. Using quantitative reverse transcription polymerase chain reaction, we studied the mRNA expression levels of resistin, adiponectin, aP<jats:sub>2<\/jats:sub>, lipoprotein lipase, PPAR\u03b3, and tumor necrosis factor\u2010\u03b1 in hMSCs undergoing adipocyte differentiation; treatment with AE decreased the expression of these adipogenic genes and decreased adipocyte differentiation. In addition, AE suppresses the differentiation of hMSCs into adipocytes by downregulating PPAR\u03b3 and C\/EBP\u03b1 expressions. AE significantly inhibited hMSCs proliferation and preadipocyte differentiation within the first 2 days of treatment, indicating that the antiadipogenic effect. \u00a9 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:291\u2013300, 2012; View this article online at<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"wileyonlinelibrary.com\">wileyonlinelibrary.com<\/jats:ext-link>. 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