Department of Internal Medicine, Pao Chien Hospital, Ping Tung City, Pingtung County, Taiwan.
Planta Med. 2012 Jun;78(10):943-50. doi: 10.1055/s-0031-1298626. Epub 2012 Jun 6.
Emodin is an active herbal component traditionally used in China for treating a variety of diseases. The aim of this study was to examine the effect of emodin on the reducing lipid accumulation in white adipose tissue of high-fat diet-fed rats, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. After being fed a high-fat diet for two weeks, rats were dosed orally with emodin (20, 40, 80 mg/kg/day) or pioglitazone (20 mg/kg/day), once daily for eight weeks. Changes in body weight, feeding pattern, serum lipids, coronary artery risk index, and atherogenic index were investigated. Subcutaneous white adipose tissues were isolated for pathology histology and Western blot analyses. Changes of triglyceride accumulation in differentiated 3 T3-L1 adipocytes were also investigated. Emodin exhibited a significant concentration-dependent decrease in the intracellular accumulation of triglyceride in 3 T3-L1 adipocytes. Emodin (80 mg/kg/day) displayed similar characteristics to pioglitazone (20 mg/kg/day) in reducing body weight gain and plasma lipid levels as well as the coronary artery risk and atherogenic indices of high-fat diet-fed rats. Emodin also caused dose related reductions in epididymal white adipose tissue sizes in high-fat diet-fed rats. Emodin and pioglitazone enhanced the phosphorylation of AMP-activated protein kinase and its primary downstream targeting enzyme, acetyl-CoA carboxylase, upregulated gene expression of carnitine palmitoyl transferase 1, and downregulated sterol regulatory element binding protein 1 and fatty acid synthase protein levels in the epididymal white adipose tissue of high-fat diet-fed rats. Our findings suggest that emodin could attenuate lipid accumulation in white adipose tissue through AMP-activated protein kinase activation.
大黄素是一种传统的中草药活性成分，在中国被用于治疗多种疾病。本研究旨在探讨大黄素对高脂饮食喂养大鼠白色脂肪组织中脂质积累的减少作用，以及对参与脂质代谢的基因表达的调节作用，以阐明其作用机制。大鼠高脂饮食喂养 2 周后，每天口服给予大黄素（20、40、80mg/kg/天）或吡格列酮（20mg/kg/天），连续 8 周。观察体重、摄食量、血脂、冠状动脉风险指数和致动脉粥样硬化指数的变化。分离皮下白色脂肪组织进行病理组织学和 Western blot 分析。还研究了分化的 3T3-L1 脂肪细胞中甘油三酯积累的变化。大黄素呈浓度依赖性地减少 3T3-L1 脂肪细胞内甘油三酯的积累。大黄素（80mg/kg/天）在降低体重增加和血浆脂质水平以及降低高脂饮食喂养大鼠的冠状动脉风险和致动脉粥样硬化指数方面与吡格列酮（20mg/kg/天）具有相似的特征。大黄素还使高脂饮食喂养大鼠的附睾白色脂肪组织大小呈剂量依赖性减少。大黄素和吡格列酮增强了 AMP 激活的蛋白激酶及其主要下游靶酶乙酰辅酶 A 羧化酶的磷酸化，上调了脂肪细胞肉碱棕榈酰转移酶 1 的基因表达，下调了固醇调节元件结合蛋白 1 和脂肪酸合酶蛋白水平。我们的研究结果表明，大黄素通过激活 AMP 激活的蛋白激酶来减轻白色脂肪组织中的脂质积累。
