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葛根素体外抗代谢综合征作用的研究

The study of anti-metabolic syndrome effect of puerarin in vitro.

作者信息

Xu Ming-En, Xiao Shang-Zhi, Sun Yong-Hong, Zheng Xiao-Xiang, Ou-Yang Yang, Guan Chen

机构信息

Department of Biomedical Engineering, Zhejiang University (Yuquan Campus), Hangzhou 310027, PR China.

出版信息

Life Sci. 2005 Nov 4;77(25):3183-96. doi: 10.1016/j.lfs.2005.03.036. Epub 2005 Jul 7.

Abstract

Puerarin is an isoflavone extracted from Chinese plant, Pueraria lobata (Wild.) Ohwi. It has been reported to have comprehensive pharmacological action in treatment of diabetes and cardiovascular diseases. The purpose of this study was to link the scattered effects of puerarin and to find the common mechanisms underlying. We investigated the effect of puerarin on the pivotal common pathogenic factors of metabolic syndrome, which includes obesity, Type II diabetes and cardiovascular diseases. Recently, a large body of evidence indicates that there is a complicated interplay among insulin resistance, adipocytes and endothelial dysfunction that links the abnormalities of metabolic syndrome. Results of present study showed that puerarin could potentiate insulin-induced preadipocyte differentiation, promote glucose-uptake of adipocytes that have been induced insulin resistance by high glucose, and prevent TNF-a-induced apoptosis and viability loss of endothelial cells. Furthermore, we found that these effects are probably due to promote PPARgamma expression and partly through inhibiting abnormal TNF-a-induced intracellular-free Ca(2+) accumulation of endothelial cells. Overall, our synthetical study links the comprehensive pharmacological actions of puerarin to the recognized common pathogenesis of metabolic syndrome, and provides a new insight into the mechanism of puerarin effect.

摘要

葛根素是从中国植物野葛(Pueraria lobata (Wild.) Ohwi)中提取的一种异黄酮。据报道,它在治疗糖尿病和心血管疾病方面具有综合药理作用。本研究的目的是将葛根素的分散作用联系起来,并找出其潜在的共同机制。我们研究了葛根素对代谢综合征关键共同致病因素的影响,代谢综合征包括肥胖、II型糖尿病和心血管疾病。最近,大量证据表明,胰岛素抵抗、脂肪细胞和内皮功能障碍之间存在复杂的相互作用,这些因素与代谢综合征的异常情况相关联。本研究结果表明,葛根素可增强胰岛素诱导的前脂肪细胞分化,促进已被高糖诱导产生胰岛素抵抗的脂肪细胞摄取葡萄糖,并防止肿瘤坏死因子-α(TNF-α)诱导的内皮细胞凋亡和活力丧失。此外,我们发现这些作用可能是由于促进过氧化物酶体增殖物激活受体γ(PPARγ)表达,部分是通过抑制TNF-α异常诱导的内皮细胞细胞内游离钙(Ca2+)蓄积。总体而言,我们的综合研究将葛根素的综合药理作用与公认的代谢综合征共同发病机制联系起来,并为葛根素作用机制提供了新的见解。

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