非酒精性脂肪肝
脂肪变性
线粒体
脂肪肝
粒体自噬
甘油三酯
线粒体生物发生
内分泌学
内科学
活性氧
氧化应激
脂滴
生物
化学
生物化学
自噬
医学
胆固醇
疾病
细胞凋亡
作者
Weijian Hang,Hongyang Shu,Zheng Wen,Jinyan Liu,Zhiyuan Jin,Zeqi Shi,Chen Chen,Dao Wen Wang
标识
DOI:10.3389/fphar.2021.636204
摘要
Rationale: Nonalcoholic fatty liver disease (NAFLD) is a kind of metabolic disease characterized by liver steatosis. Excessive reactive oxygen species (ROS) originating from dysfunctional mitochondria is the major pathophysiological contributor in the development of NAFLD and is thought to be a promising therapeutic target. A few reports demonstrate the antioxidative treatments for NAFLD. Methods: Male C57 mice were fed on a normal chow diet (ND) or high-fat diet (HFD) for 8 weeks. PBS or N-acetyl cysteine (NAC) was gavaged to mice. LO2 human liver cell line treated with palmitic acid (PA) was applied as a cellular model. Western blot, immunofluorescence, biochemistry assay, and pathological staining were used to investigate the mechanism of suppressing lipid accumulation of NAC. Results: NAC treatment was able to prevent HFD-induced NAFLD, as evidenced by less hepatic triglyceride accumulation and lipid droplet formation compared with that of mice in the HFD group. NAC could preserve mitochondrial function by inhibiting excessive mitophagy and promoting mitochondria biogenesis to prevent ROS production. NAC also activated Sirt1 and preserved its protein level and subsequently promoted mitochondria biogenesis via deacetylating PGC1a. Conclusion: We demonstrated that NAC may be an effective drug to treat NAFLD, which was related to its antioxidative and mitochondrial protective effect.
科研通智能强力驱动
Strongly Powered by AbleSci AI