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大黄素通过激活 PPARγ对高脂饮食喂养和小剂量链脲佐菌素诱导的糖尿病小鼠的抗糖尿病作用。

Anti-diabetic effects of emodin involved in the activation of PPARgamma on high-fat diet-fed and low dose of streptozotocin-induced diabetic mice.

机构信息

College of Life Sciences, Graduate University of Chinese Academy of Sciences, No. 19 A Yu Quan Road, Beijing, China.

出版信息

Fitoterapia. 2010 Apr;81(3):173-7. doi: 10.1016/j.fitote.2009.08.020. Epub 2009 Aug 20.

DOI:10.1016/j.fitote.2009.08.020
PMID:19699280
Abstract

Rheum palmatum Linn has been widely applied in the clinical treatment of diabetes mellitus. It has been found that emodin as the major bioactive component of R. palmatum L exhibits the competency to activate peroxisomal proliferator-activated receptor-gamma (PPARgamma) in vitro. So the aim of this study was to evaluate the anti-diabetic effects of emodin through the activation of PPARgamma on high-fat diet-fed and low dose of streptozotocin (STZ)-induced diabetic mice. The diabetic mice were intraperitoneally injected with emodin for three weeks. No changes of food consumption and the body weight in emodin-treated mice were monitored daily during the entire experiment. At the end of experiment, the levels of blood glucose, triglyceride and total cholesterol in serum were significantly decreased after emodin treatment. However, serum high-density lipoprotein cholesterol (HDLc) concentration was significantly elevated. The glucose tolerance and insulin sensitivity in emodin-treated group were significantly improved. Furthermore, the results of quantitative RT-PCR analysis showed that emodin significantly elevated the mRNA expression level of PPARgamma and regulated the mRNA expressions of LPL, FAT/CD36, resistin and FABPs (ap2) in liver and adipocyte tissues. No effects on the mRNA expressions of PPARalpha and PPARalpha-target genes were observed. Taken together, the results suggested that the activation of PPARgamma and the modulation of metabolism-related genes were likely involved in the anti-diabetic effects of emodin.

摘要

拳参已被广泛应用于糖尿病的临床治疗中。研究发现,大黄素作为拳参的主要生物活性成分,在体外具有激活过氧化物酶体增殖物激活受体-γ(PPARγ)的能力。因此,本研究旨在通过激活 PPARγ来评价大黄素对高脂饮食喂养和低剂量链脲佐菌素(STZ)诱导的糖尿病小鼠的抗糖尿病作用。糖尿病小鼠连续 3 周腹腔注射大黄素。整个实验过程中,每天监测大黄素处理组小鼠的食物消耗和体重变化。实验结束时,大黄素治疗后血清中血糖、甘油三酯和总胆固醇水平显著降低,而高密度脂蛋白胆固醇(HDLc)浓度显著升高。大黄素处理组的葡萄糖耐量和胰岛素敏感性显著改善。此外,定量 RT-PCR 分析结果表明,大黄素显著上调了 PPARγ的 mRNA 表达水平,并调节了肝脏和脂肪组织中 LPL、FAT/CD36、抵抗素和 FABPs(ap2)的 mRNA 表达。未观察到对 PPARα和 PPARα靶基因的 mRNA 表达有影响。综上所述,这些结果表明,大黄素的抗糖尿病作用可能与激活 PPARγ和调节代谢相关基因有关。

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