Li Jinmei, Ding Lili, Song Baoliang, Xiao Xu, Qi Meng, Yang Qiaoling, Yang Qiming, Tang Xiaowen, Wang Zhengtao, Yang Li
(a)The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Shanghai Key Laboratory of Complex Prescriptions, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
(a)The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the State Administration of TCM (SATCM) Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Shanghai Key Laboratory of Complex Prescriptions, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; Center for Chinese Medical Therapy and Systems Biology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Eur J Pharmacol. 2016 Jan 5;770:99-109. doi: 10.1016/j.ejphar.2015.11.045. Epub 2015 Nov 25.
Currently, obesity has become a worldwide epidemic associated with Type 2 diabetes, dyslipidemia, cardiovascular disease and chronic metabolic diseases. Emodin is one of the active anthraquinone derivatives from Rheum palmatum and some other Chinese herbs with anti-inflammatory, anticancer and hepatoprotective properties. In the present study, we investigated the anti-obesity effects of emodin in obese mice and explore its potential pharmacological mechanisms. Male C57BL/6 mice were fed with high-fat diet for 12 weeks to induce obesity. Then the obese mice were divided into four groups randomly, HFD or emodin (40mg/kg/day and 80mg/kg/day) or lovastatin (30mg/kg/ day) for another 6 weeks. Body weight and food intake were recorded every week. At the end of the treatment, the fasting blood glucose, glucose and insulin tolerance test, serum and hepatic lipid levels were assayed. The gene expressions of liver and adipose tissues were analyzed with a quantitative PCR assay. Here, we found that emodin inhibited sterol regulatory element-binding proteins (SREBPs) transactivity in huh7 cell line. Furthermore, emodin (80mg/kg/day) treatment blocked body weight gain, decreased blood lipids, hepatic cholesterol and triglyceride content, ameliorated insulin sensitivity, and reduced the size of white and brown adipocytes. Consistently, SREBP-1 and SREBP-2 mRNA levels were significantly reduced in the liver and adipose tissue after emodin treatment. These data demonstrated that emodin could improve high-fat diet-induced obesity and associated metabolic disturbances. The underlying mechanism is probably associated with regulating SREBP pathway.
目前，肥胖已成为一种全球性的流行病，与2型糖尿病、血脂异常、心血管疾病及慢性代谢性疾病相关。大黄素是掌叶大黄及其他一些中药中的活性蒽醌衍生物之一，具有抗炎、抗癌及肝脏保护特性。在本研究中，我们调查了大黄素对肥胖小鼠的抗肥胖作用，并探索其潜在的药理机制。雄性C57BL/6小鼠喂食高脂饮食12周以诱导肥胖。然后将肥胖小鼠随机分为四组，分别给予高脂饮食或大黄素（40mg/kg/天和80mg/kg/天）或洛伐他汀（30mg/kg/天），持续另外6周。每周记录体重和食物摄入量。治疗结束时，测定空腹血糖、葡萄糖和胰岛素耐量试验、血清及肝脏脂质水平。采用定量PCR分析肝脏和脂肪组织的基因表达。在此，我们发现大黄素在huh7细胞系中抑制固醇调节元件结合蛋白（SREBPs）的转录活性。此外，大黄素（80mg/kg/天）治疗可阻止体重增加，降低血脂、肝脏胆固醇和甘油三酯含量，改善胰岛素敏感性，并减小白色和棕色脂肪细胞的大小。一致地，大黄素治疗后肝脏和脂肪组织中SREBP-1和SREBP-2的mRNA水平显著降低。这些数据表明，大黄素可改善高脂饮食诱导的肥胖及相关代谢紊乱。其潜在机制可能与调节SREBP途径有关。
