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首页> 外文期刊>The American journal of Chinese medicine >Houttuynia cordata attenuates lipid accumulation via activation of AMP-activated protein kinase signaling pathway in HepG2 cells
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Houttuynia cordata attenuates lipid accumulation via activation of AMP-activated protein kinase signaling pathway in HepG2 cells

机译:鱼腥草通过激活AMP激活的蛋白激酶信号通路在HepG2细胞中减轻脂质积累

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Houttuynia cordata (H. cordata) from the family Saururaceae is a perennial herb native to Southeast Asia. It possesses a range of medicinal properties to treat several disease symptoms including allergic inflammation and anaphylaxis. In the present investigation, we provided the molecular mechanisms underlying the role of H. cordata extract (HCE) in the prevention of high glucose-induced lipid accumulation in human HepG2 hepatocytes. HepG2 cells were pre-treated with various concentrations of HCE (0, 10, 20, 40, and 80 μg/mL) and treated with serum-free medium with normal glucose (5 mM) for 1 h, followed by exposure to high glucose (25 mM D-glucose) for 24 h. HCE significantly and dose-dependently attenuated lipid accumulation in human HepG2 hepatocytes when exposed to high glucose (25 mM D-glucose) (p < 0.05, p < 0.01 and p < 0.001 at 20, 40, and 80 μg/mL concentrations, respectively). Further, HCE attenuated the expression of fatty acid synthase (FAS), sterol regulatory element-binding protein-1 and glycerol 3-phosphate acyltransferases (GPATs). The adenosine monophosphate-activated protein kinase (AMPK) was also activated by HCE treatment when exposed to high glucose (25 mM D-glucose) in human HepG2 hepatocytes. This study suggests the hypolipidemic effects of HCE by the inhibition of lipid biosynthesis mediated through AMPK signaling, which may play an active role and can be developed as an anti-obesity agent.
机译:鱼腥草科的鱼腥草是一种多年生草本植物,原产于东南亚。它具有多种医学特性,可以治疗多种疾病症状,包括变态反应性炎症和过敏反应。在目前的研究中,我们提供了潜在的分子机制,在预防HepG2肝细胞中高糖诱导的脂质蓄积中,H。cordata提取物(HCE)发挥了作用。用不同浓度的HCE(0、10、20、40和80μg/ mL)预处理HepG2细胞,并用含正常葡萄糖(5 mM)的无血清培养基处理1 h,然后暴露于高葡萄糖(25 mM D-葡萄糖)处理24小时。当暴露于高葡萄糖(25 mM D-葡萄糖)(分别在20、40和80μg/ mL浓度下分别为p <0.05,p <0.01和p <0.001)时,HCE显着且剂量依赖性地减弱了人类HepG2肝细胞中的脂质积累)。此外,HCE减弱了脂肪酸合酶(FAS),固醇调节元件结合蛋白1和3-磷酸甘油酰基转移酶(GPAT)的表达。当暴露于人HepG2肝细胞中的高葡萄糖(25 mM D-葡萄糖)时,腺苷一磷酸激活的蛋白激酶(AMPK)也被HCE处理激活。这项研究表明,HCE的降血脂作用是通过抑制通过AMPK信号传导介导的脂质生物合成来实现的,该作用可能起积极作用,并可以发展为抗肥胖药。

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