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首页> 外文期刊>Drug Design, Development and Therapy >Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy
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Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy

机译：Galangin通过促进自噬改善了小鼠的非酒精脂肪肝疾病

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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.
机译：背景：以前的研究表明，姜黄素衍生物可以改善非酒精脂肪肝病（NAFLD）中发生的肝组织的脂肪变性。然而，这种改进的具体机制仍然不清楚。从预防和治疗的角度来看，我们检查了姜黄素衍生物的Galangin是否可以通过诱导自噬减少与NAFLD的肝组织脂肪变性。方法：将C57BL / 6J小鼠随机分配给预防组（同时给予Galangin和HFD）或治疗组（喂养HFD后给予Galangin）。预防组在加入HFD的同时用Galangin（100mg / kg / d）或等体积的正常盐水（ns）处理。将一些小鼠用自噬抑制剂（3-甲基腺嘌呤，3-mA; 30mg / kg / biwk，I.p.）处理，同时喂养HFD和Galangin。在含有游离脂肪酸和Galangin的DMEM培养基中培养HepG2细胞。结果：发现Galangin降低通过在预防和治疗水平患有HFD而引起的肝组织的脂肪变性，并且该效果可能与肝细胞自噬的增强有关。通过3-mA对自噬的抑制阻断了Galangin对肝脏脂肪变性的保护作用。在细胞水平下，加兰林减少脂质积累，增强了肝细胞自噬水平。结论：体外和体内研究表明，Galangin不能改善预先存在的肝脏脂肪，还可以通过促进肝细胞自噬，防止狭窄的发展。

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