Henan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, Henan 475004, China.
School of Stomatology, Henan University, Kaifeng, Henan 475004, China.
Oxid Med Cell Longev. 2021 Apr 17;2021:5599997. doi: 10.1155/2021/5599997. eCollection 2021.
Nonalcoholic fatty liver disease (NAFLD) represents one of the most common chronic liver diseases in the world. It has been reported that epigallocatechin-3-gallate (EGCG) plays important biological and pharmacological roles in mammalian cells. Nevertheless, the mechanism underlying the beneficial effect of EGCG on the progression of NAFLD has not been fully elucidated. In the present study, the mechanisms of action of EGCG on the growth, apoptosis, and autophagy were examined using oleic acid- (OA-) treated liver cells and the high-fat diet- (HFD-) induced NAFLD mouse model. Administration of EGCG promoted the growth of OA-treated liver cells. EGCG could reduce mitochondrial-dependent apoptosis and increase autophagy possibly via the reactive oxygen species- (ROS-) mediated mitogen-activated protein kinase (MAPK) pathway in OA-treated liver cells. In line with findings, our study verified that treatment with EGCG attenuated HFD-induced NAFLD through reduction of apoptosis and promotion of autophagy. EGCG can alleviate HFD-induced NAFLD possibly by decreasing apoptosis and increasing autophagy via the ROS/MAPK pathway. EGCG may be a promising agent for the treatment of NAFLD.
非酒精性脂肪性肝病 (NAFLD) 是世界上最常见的慢性肝病之一。有报道称，表没食子儿茶素没食子酸酯 (EGCG) 在哺乳动物细胞中具有重要的生物学和药理学作用。然而，EGCG 对 NAFLD 进展的有益作用的机制尚未完全阐明。在本研究中，使用油酸 (OA-) 处理的肝细胞和高脂肪饮食 (HFD-) 诱导的 NAFLD 小鼠模型研究了 EGCG 对细胞生长、凋亡和自噬的作用机制。EGCG 的给药促进了 OA 处理的肝细胞的生长。EGCG 可能通过 ROS 介导的丝裂原激活蛋白激酶 (MAPK) 通路减少线粒体依赖性凋亡并增加自噬，从而减少 OA 处理的肝细胞中的凋亡并增加自噬。与研究结果一致，我们的研究证实，EGCG 通过减少凋亡和促进自噬来减轻 HFD 诱导的 NAFLD。EGCG 可能通过 ROS/MAPK 通路减少凋亡和增加自噬来减轻 HFD 诱导的 NAFLD。EGCG 可能是治疗 NAFLD 的一种有前途的药物。
