Key result
Tetrahydropalmatine reduces preclinical lipid accumulation by activating autophagy via the AMPK-mTOR-Sirt1 axis.
Why the study?
The hepatoprotective effects and mechanisms of tetrahydropalmatine (THP) in non-alcoholic fatty liver disease (NAFLD) were not systematically investigated.
Tetrahydropalmatine demonstrates hepatoprotective effects in NAFLD models by reducing lipid accumulation through autophagy activation and lipid metabolic reprogramming.
May support preclinical NAFLD research; leaves open translation to human therapy pending clinical trials.
ETHNOPHARMACOLOGICAL RELEVANCE: Corydalis yanhusuo W. T. Wang (C. yanhusuo) is a traditional Chinese medicinal herb commonly used in clinical practice for liver protection and lipid-lowering. Tetrahydropalmatine (THP), one of the major active components of C. yanhusuo, has been demonstrated to exert significant anti-inflammatory and lipid-lowering effects. AIM OF THE STUDY: This study aimed to systematically investigate the effects of THP on non-alcoholic fatty liver disease (NAFLD) through both in vivo and in vitro experiments, and to elucidate its potential underlying mechanisms. MATERIALS AND METHODS: We constructed palmitic acid/oleic acid (PO)-induced HepG2 cell and high-fat diet (HFD) mouse models, combined with metabolomics, network pharmacology, Seahorse analysis, and validation using autophagy/AMPK modulators. RESULTS: THP significantly reduced lipid accumulation in vitro and in vivo, while CQ attenuated its lipid-lowering effect, indicating autophagy dependence. Network pharmacology identified MTOR and SIRT1 as central nodes. THP increased AMPK phosphorylation, inhibited mTOR, and upregulated ATG5, ATG9, Beclin 1, and LC3-II, restoring autophagic flux. Metabolomic analysis revealed significant remodeling of glycerophospholipid, linoleic acid, and glutathione metabolism, optimizing membrane lipid composition for autophagosome formation and enhancing antioxidant capacity. Seahorse analysis showed that THP not only significantly reduced the extracellular acidification rate (ECAR) but also enhanced both basal and maximal oxygen consumption rates (OCR). In addition, THP upregulated Sirt1 expression and the p-ACC/ACC ratio, while downregulating SREBP-1c and FAS, thereby inhibiting lipid deposition. CONCLUSION: THP exerts hepatoprotective effects in NAFLD by activating autophagy and reprogramming lipid metabolism through the AMPK-mTOR-Sirt1 axis.
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Guo et al. (2026) studied non-alcoholic fatty liver disease (NAFLD). Tetrahydropalmatine (THP) was evaluated on lipid accumulation. Tetrahydropalmatine significantly reduced lipid accumulation in vitro and in vivo by activating autophagy and reprogramming lipid metabolism through the AMPK-mTOR-Sirt1 axis.
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