Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway.
Hydrogen Sulfide Attenuates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease by Inhibiting Apoptosis and Promoting Autophagy via Reactive Oxygen Species/Phosphatidylinositol 3-Kinase/AKT/Mammalian Target of Rapamycin Signaling Pathway.
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硫化氢通过活性氧/磷脂酰肌醇 3-激酶/AKT/雷帕霉素信号通路的哺乳动物靶标抑制细胞凋亡和促进自噬，从而减轻高脂饮食诱发的非酒精性脂肪肝
DOI：
10.3389/fphar.2020.585860
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发表时间：
2020
影响因子：
5.6
通讯作者：
Li Y
中科院分区：
文献类型：
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作者：
Wu D;Zhong P;Wang Y;Zhang Q;Li J;Liu Z;Ji A;Li Y
非酒精性脂肪性肝病（NAFLD）是一种常见的慢性肝病。硫化氢（H2S）参与了广泛的生理和病理过程。然而，H2S在NAFLD发展中的作用机制尚未完全阐明。在此，在用油酸（OA）处理的肝细胞中观察到H2S水平降低。H2S的管理增加OA处理的细胞的增殖。结果表明，H2S通过活性氧介导的PI 3 K/AKT/mTOR级联反应抑制OA诱导的细胞凋亡，促进细胞自噬。此外，H2S的施用通过抑制细胞凋亡和促进自噬来减轻高脂饮食（HFD）诱导的NAFLD。提示H2S可通过ROS/PI 3 K/AKT/mTOR信号通路调节细胞凋亡和自噬，从而减轻HFD诱导的NAFLD。新型H2S释放供体可能具有治疗NAFLD的治疗潜力。
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide. Hydrogen sulfide (H2S) is involved in a wide range of physiological and pathological processes. Nevertheless, the mechanism of action of H2S in NAFLD development has not been fully clarified. Here, the reduced level of H2S was observed in liver cells treated with oleic acid (OA). Administration of H2S increased the proliferation of OA-treated cells. The results showed that H2S decreased apoptosis and promoted autophagy through reactive oxygen species (ROS)-mediated phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) cascade in OA-treated cells. In addition, administration of H2S relieved high-fat diet (HFD)-induced NAFLD via inhibition of apoptosis and promotion of autophagy. These findings suggest that H2S could ameliorate HFD-induced NAFLD by regulating apoptosis and autophagy through ROS/PI3K/AKT/mTOR signaling pathway. Novel H2S-releasing donors may have therapeutic potential for the treatment of NAFLD.
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影响因子：
5.3
作者：
Chen L;Liu P;Feng X;Ma C
通讯作者：
Ma C
影响因子：
11.4
作者：
Lee, You-Kyung;Jun, Yong-Woo;Lee, Jin-A
通讯作者：
Lee, Jin-A
影响因子：
18.9
作者：
Mani, Sarathi;Li, Hongzhu;Wang, Rui
通讯作者：
Wang, Rui
影响因子：
37.8
作者：
Mani, Sarathi;Li, Hongzhu;Wang, Rui
通讯作者：
Wang, Rui
影响因子：
9
作者：
通讯作者：
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