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枸杞粗提物通过激活AMPK抑制SREBP-1c表达并预防饮食诱导的脂肪肝。

Crude extracts from Lycium barbarum suppress SREBP-1c expression and prevent diet-induced fatty liver through AMPK activation.

作者信息

Li Wang, Li Yan, Wang Qing, Yang Yi

机构信息

Biochemistry and Molecular Biology, Ningxia Medical University, Yinchuan 750004, China.

Biochemistry and Molecular Biology, Ningxia Medical University, Yinchuan 750004, China ; Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Yinchuan 750004, China.

出版信息

Biomed Res Int. 2014;2014:196198. doi: 10.1155/2014/196198. Epub 2014 Jun 10.

Abstract

Lycium barbarum polysaccharide (LBP) is well known in traditional Chinese herbal medicine that, has beneficial effects. Previous study reported that LBP reduced blood glucose and serum lipids. However, the underlying LBP-regulating mechanisms remain largely unknown. The main purpose of this study was to investigate whether LBP prevented fatty liver through activation of adenosine monophosphate-activated protein kinase (AMPK) and suppression of sterol regulatory element-binding protein-1c (SREBP-1c). Male C57BL/6J mice were fed a low-fat diet, high-fat diet, or 100 mg/kg LBP-treatment diet for 24 weeks. HepG2 cells were treated with LBP in the presence of palmitic acid. In our study, LBP can improve body compositions and lipid metabolic profiles in high-fat diet-fed mice. Oil Red O staining in vivo and in vitro showed that LBP significantly reduced hepatic intracellular triacylglycerol accumulation. H&E staining also showed that LBP can attenuate liver steatosis. Hepatic genes expression profiles demonstrated that LBP can activate the phosphorylation of AMPK, suppress nuclear expression of SREBP-1c, and decrease protein and mRNA expression of lipogenic genes in vivo or in vitro. Moreover, LBP significantly elevated uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) expression of brown adipose tissue. In summary, LBP possesses a potential novel treatment in preventing diet-induced fatty liver.

摘要

枸杞多糖(LBP)在传统中药中广为人知,具有有益作用。先前的研究报道LBP可降低血糖和血脂。然而,LBP的潜在调节机制在很大程度上仍不清楚。本研究的主要目的是探讨LBP是否通过激活单磷酸腺苷激活蛋白激酶(AMPK)和抑制固醇调节元件结合蛋白-1c(SREBP-1c)来预防脂肪肝。将雄性C57BL/6J小鼠分别喂食低脂饮食、高脂饮食或100mg/kg LBP处理饮食24周。在棕榈酸存在的情况下,用LBP处理HepG2细胞。在我们的研究中,LBP可以改善高脂饮食喂养小鼠的身体组成和脂质代谢谱。体内和体外油红O染色显示,LBP显著降低肝脏细胞内三酰甘油的积累。苏木精-伊红染色也显示LBP可以减轻肝脏脂肪变性。肝脏基因表达谱表明,LBP可以在体内或体外激活AMPK的磷酸化,抑制SREBP-1c的核表达,并降低脂肪生成基因的蛋白质和mRNA表达。此外,LBP显著提高棕色脂肪组织中解偶联蛋白-1(UCP1)和过氧化物酶体增殖物激活受体-γ共激活因子-1α(PGC-1α)的表达。总之,LBP在预防饮食诱导的脂肪肝方面具有潜在的新治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b415/4071778/1832df1db9fe/BMRI2014-196198.001.jpg

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