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It has been reported that epigallocatechin\u20103\u2010gallate (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\u2010 (OA\u2010) treated liver cells and the high\u2010fat diet\u2010 (HFD\u2010) induced NAFLD mouse model. Administration of EGCG promoted the growth of OA\u2010treated liver cells. EGCG could reduce mitochondrial\u2010dependent apoptosis and increase autophagy possibly via the reactive oxygen species\u2010 (ROS\u2010) mediated mitogen\u2010activated protein kinase (MAPK) pathway in OA\u2010treated liver cells. In line with <jats:italic>in vitro<\/jats:italic> findings, our <jats:italic>in vivo<\/jats:italic> study verified that treatment with EGCG attenuated HFD\u2010induced NAFLD through reduction of apoptosis and promotion of autophagy. EGCG can alleviate HFD\u2010induced NAFLD possibly by decreasing apoptosis and increasing autophagy via the ROS\/MAPK pathway. EGCG may be a promising agent for the treatment of NAFLD.<\/jats:p>","DOI":"10.1155\/2021\/5599997","type":"journal-article","created":{"date-parts":[[2021,4,18]],"date-time":"2021-04-18T01:20:05Z","timestamp":1618708805000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Epigallocatechin\u20103\u2010Gallate Alleviates High\u2010Fat Diet\u2010Induced Nonalcoholic Fatty Liver Disease via Inhibition of Apoptosis and Promotion of Autophagy through the ROS\/MAPK Signaling 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