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白藜芦醇通过Sirt1-FOXO1信号通路抑制脂肪变性细胞模型中SREBP1的表达。

Resveratrol inhibits the expression of SREBP1 in cell model of steatosis via Sirt1-FOXO1 signaling pathway.

作者信息

Wang Guang-Li, Fu Yu-Cai, Xu Wen-Can, Feng Ya-Qing, Fang Shi-Rong, Zhou Xiao-Hui

机构信息

Department of Lemology, The First Affiliated Hospital of Shantou University Medical College, 57 Changping Road, Shantou 515041, PR China.

出版信息

Biochem Biophys Res Commun. 2009 Mar 13;380(3):644-9. doi: 10.1016/j.bbrc.2009.01.163. Epub 2009 Jan 31.

DOI:10.1016/j.bbrc.2009.01.163
PMID:19285015
Abstract

Recent studies in mice have shown that resveratrol can protect the liver from fat accumulation induced by high fat diet. However, the exact mechanism is largely unknown. To explore the possible mechanism, we investigated the anti-lipogenic effect of resveratrol in vitro model. Oil Red O staining revealed that resveratrol could significantly ameliorate the excessive triglyceride accumulation in HepG2 cells induced by palmitate. The results of RT-PCR and Western blotting showed that resveratrol upregulated the expression of Sirt1 and forkhead box O1 (FOXO1), whereas downregulated the expression of sterol regulatory element binding protein1 (SREBP1). Moreover, resveratrol was shown to inhibit the activity of SREBP1, as evaluated by immunofluorescence assay. Our results suggest that resveratrol may attenuate fat deposition by inhibiting SREBP1 expression via Sirt1-FOXO1 pathway and thus may have application for the treatment of NAFLD.

摘要

最近在小鼠身上的研究表明,白藜芦醇可以保护肝脏免受高脂饮食诱导的脂肪堆积。然而,确切机制在很大程度上尚不清楚。为了探究可能的机制,我们在体外模型中研究了白藜芦醇的抗脂肪生成作用。油红O染色显示,白藜芦醇可以显著改善棕榈酸诱导的HepG2细胞中过量的甘油三酯堆积。RT-PCR和蛋白质免疫印迹结果表明,白藜芦醇上调了沉默调节蛋白1(Sirt1)和叉头框蛋白O1(FOXO1)的表达,而下调了固醇调节元件结合蛋白1(SREBP1)的表达。此外,通过免疫荧光测定评估,白藜芦醇显示出抑制SREBP1的活性。我们的结果表明,白藜芦醇可能通过Sirt1-FOXO1途径抑制SREBP1表达来减轻脂肪沉积,因此可能在非酒精性脂肪性肝病的治疗中具有应用价值。

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