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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 Department of Histology, College of Veterinary Medicine, Kyungpook National University, Daegu-si 41566, North Gyeongsang-do, Republic of Korea; [cmjdgt@naver.com](cmjdgt@naver.com) (M.-J.J.); [lifelove@korea.kr](lifelove@korea.kr) (S.J.H.); [newmoon93@daum.net](newmoon93@daum.net) (M.-G.S.); [jun25253337@gmail.com](jun25253337@gmail.com) (J.-H.L.)  \n2 BTC Corporation, Gwacheon Creation Tower, 46, Gwacheon-daero 7-gil, Gwacheon-si 13840, Gyeonggi-do, Republic of Korea; [jwlee@btcbio.com](jwlee@btcbio.com) (J.W.L.); [kyh@btcbio.com](kyh@btcbio.com) (Y.H.K.); [dogulas.kim@btcbio.com](dogulas.kim@btcbio.com) (Y.K.)  \n* [Correspondence: psj26@knu.ac.kr](Correspondence: psj26@knu.ac.kr); Tel.: +82-53-950-5970 † These authors contributed equally to this work.  \nAbstract  \nBackground: Non-alcoholic steatohepatitis (NASH) lacks approved pharmacotherapies despite affecting approximately 25% of the global population. Agrimonia pilosa, a traditional herb with anti-inflammatory and antioxidant properties, remains unexplored for NASH treatment. Objective: This study investigated the hepatoprotective effects and mechanisms of Agrimonia pilosa extract (APE) in NASH models. Methods: HepG2 cells were treated with free fatty acids (0.125 mM) and APE (+12.5–50 µg/mL) . C57BL/6J mice received a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 12 weeks with APE (25–100 mg/kg/day), silymarin (100 mg/kg/day), or luteolin (20 mg/kg/day) . Lipid accumulation, liver enzymes, histopathology, and molecular markers were assessed. Results: APE dose-dependently reduced lipid accumulation in FFA-treated cells, suppressed lipogenic factors (SREBF1, CEBPA, and PPARG), and upregulated fatty acid oxidation enzymes (CPT1A and PPARA) via AMPK/SIRT1 activation. In NASH mice, APE (100 mg/kg) significantly decreased serum ALT (160.0 ± 49.1 vs. 311.2 ± 66.7 U/L) and AST (96.0 ± 18.7 vs. 219.0 ± 55.7 U/L, p \u003C 0.001), reduced hepatic macrophage infiltration by 68%, and substantially attenuated inflammatory markers (Ccl2, Tnf, and IL6), oxidative stress indicators (NRF2, HMOX1, and CYBB), and fibrogenic markers (ACTA2, COL1A1, and TGFB1) by 83–85%(p \u003C 0.001) . Collagen deposition decreased from 5.63 ± 0.39% to 1.54 ± 0.03%(p \u003C 0.001) . Conclusions: APE exerts potent hepatoprotective effects through multi-targeted modulation of lipid metabolism, inflammation, oxidative stress, and fibrosis via AMPK/SIRT1 pathway activation, supporting its potential as a natural therapeutic intervention for NASH.  \nKeywords: non-alcoholic steatohepatitis; Agrimonia pilosa; lipid metabolism; inflammation; oxidative stress; AMPK/SIRT1 signaling pathway  \n1. Introduction  \nNon-alcoholic fatty liver disease (NAFLD) represents a metabolic disorder affecting approximately 25% of the global population, making it a significant public health challenge [1,2] . NAFLD encompasses a disease spectrum ranging from simple hepatic steatosisto non-alcoholic steatohepatitis (NASH), characterized by hepatic inflammation and fibrosis in the absence of excessive alcohol consumption. Without therapeutic intervention, NASH  \nmay progress to life-threatening conditions, including compensated and decompensated cirrhosis and hepatocellular carcinoma [1,3] . Additionally, NASH demonstrates strong associations with metabolic complications such as obesity, dyslipidemia, insulin resistance, and chronic kidn","cbCaieoJwewUNdDf","https://ap.wps.com/l/cbCaieoJwewUNdDf","pdf",4179573,24,"English","# Abstract\n## Background\n## Objective\n## Methods\n## Results\n## Conclusions\n# 1. Introduction","[{\"question\":\"Why is NASH considered a major unmet medical need?\",\"answer\":\"NASH lacks approved pharmacotherapies even though it affects a large portion of the global population. The disease can progress to severe outcomes such as cirrhosis and hepatocellular carcinoma.\"},{\"question\":\"How was Agrimonia pilosa extract (APE) tested in this study?\",\"answer\":\"HepG2 cells were treated with free fatty acids and APE at different concentrations. Mice received a choline-deficient, L-amino acid-defined high-fat diet (CDAHFD) for 12 weeks along with APE or comparator agents.\"},{\"question\":\"What mechanisms does APE act through according to the reported results?\",\"answer\":\"APE dose-dependently reduced lipid accumulation, suppressed lipogenic factors, and increased fatty acid oxidation enzymes through AMPK/SIRT1 activation. It also attenuated inflammation, oxidative stress, and fibrosis-related markers.\"}]","Agrimonia pilosa Extract Alleviates CDAHFD-Induced Non-Alcoholic Steatohepatitis and Fibrosis in Mice | PDF",1790771814]