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Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy.
Drug Design, Development and Therapy ( IF 4.7 ) Pub Date : 2020-08-19 , DOI: 10.2147/dddt.s258187
Xinxu Zhang 1 , Yuanyuan Deng 1 , Juan Xiang 1 , Huixia Liu 1 , Jiani Zhang 1 , Jie Liao 1 , Ke Chen 1 , Bo Liu 1 , Jun Liu 1 , Ying Pu 1
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Background: Previous studies have shown that curcumin derivatives can improve the fatty degeneration of liver tissue that occurs in nonalcoholic fatty liver disease (NAFLD). However, the specific mechanism for that improvement remains unclear. We examined whether the curcumin derivative galangin could reduce the fatty degeneration of liver tissue in mice with NAFLD by inducing autophagy, from the perspective of both prevention and treatment.
Methods: C57BL/6J mice were randomly assigned to a prevention group (given galangin and a HFD simultaneously) or a treatment group (given galangin after being fed an HFD). The prevention group was treated with galangin (100 mg/kg/d) or an equal volume of normal saline (NS) while being fed an HFD. Some mice were treated with an autophagy inhibitor (3-methyladenine, 3-MA; 30 mg/kg/biwk, i.p.) while being fed an HFD and galangin. HepG2 cells were cultured in DMEM medium containing both free fatty acids and galangin.
Results: Galangin was found to reduce the fatty degeneration of liver tissue induced by eating an HFD at both the prevention and treatment levels, and that effect might be related to an enhancement of hepatocyte autophagy. Inhibition of autophagy by 3-MA blocked the protective effect of galangin on hepatic steatosis. At the cellular level, galangin reduced lipid accumulation and enhanced the level of hepatocyte autophagy.
Conclusion: In vitro and in vivo studies showed that galangin cannot only improve pre-existing hepatic steatosis but also prevent the development of stenosis by promoting hepatocyte autophagy.



中文翻译:

高良姜素通过促进自噬改善了小鼠的非酒精性脂肪肝。

背景:以前的研究表明,姜黄素衍生物可以改善发生在非酒精性脂肪肝(NAFLD)中的肝组织脂肪变性。然而,这种改善的具体机制仍不清楚。我们从预防和治疗的角度研究了姜黄素衍生物高良姜素是否可以通过诱导自噬来减少 NAFLD 小鼠肝组织的脂肪变性。
方法:C57BL/6J 小鼠被随机分配到预防组(同时给予高良姜素和 HFD)或治疗组(在喂食 HFD 后给予高良姜素)。预防组在喂食 HFD 的同时用高良姜素 (100 mg/kg/d) 或等体积的生理盐水 (NS) 治疗。一些小鼠在喂食 HFD 和高良姜素的同时用自噬抑制剂(3-甲基腺嘌呤,3-MA;30 mg/kg/biwk,ip)治疗。HepG2细胞在含有游离脂肪酸和高良姜素的DMEM培养基中培养。
结果:发现高良姜素可以在预防和治疗水平上减少食用 HFD 引起的肝组织脂肪变性,这种作用可能与肝细胞自噬的增强有关。3-MA对自噬的抑制阻断了高良姜素对肝脂肪变性的保护作用。在细胞水平上,高良姜素减少脂质积累并提高肝细胞自噬水平。
结论:体外和体内研究表明,高良姜素不仅可以改善已有的肝脂肪变性,而且可以通过促进肝细胞自噬来预防狭窄的发展。

更新日期:2020-08-19
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