Article3 Biotech2025
Yinchen lipid-lowering tea attenuates lipid deposition in a fatty liver model by regulating mitochondrial dysfunction through activation of AdipoR1/AMPK/SIRT1 signaling.
Article in 3 Biotech, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The LKB1-AMPK pathway in NAFLD: molecular mechanisms and therapeutic implications.Journal of physiology and biochemistry · 2026Review
- Glucagon-Like Peptide-2 Ameliorates Lipid Metabolism in Metabolic Dysfunction-Associated Steatotic Liver Disease Through the Adiponectin-Adiponectin Receptor-Mediated AMPK/PPARalpha Pathway.Physiological research · 2026Article
- Natural products intervene in non-alcoholic fatty liver disease by regulating the AMPK signaling pathway: preclinical evidence and mechanism.Frontiers in pharmacology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the ameliorative effects of Yinchen lipid-lowering tea (YCLLT) on Non-alcoholic fatty liver disease (NAFLD), the specific mechanism involved was also studied. We modeled hepatocellular steatosis with HepG2 cells and intervened with different concentrations of YCLLT-containing serum. Lipid deposition was assessed by oil red O staining and AdipoR1 expression was analyzed by Western blot. The hepatocyte steatosis model was further treated with YCLLT-containing serum and/or silencing AdipoR1. Lipid deposition was observed by oil red O staining. Flow cytometry was used to detect apoptosis and mitochondrial membrane potential. The levels of TNF-α, IL-6, MDA, 8-OHdG, and ATP were analyzed by ELISA or the corresponding kits. The mitochondrial structure was observed by transmission electron microscopy. The expression of AdipoR1/AMPK/SIRT1 signaling pathway factors was analyzed by Western blot, and co-localization of SIRT1 and immunofluorescence. The results revealed that YCLLT attenuated lipid deposition, inhibited the levels of inflammatory factors TNF-α and IL-6, reduced the levels of MDA and 8-OHdG, up-regulated the ATP content and mitochondrial membrane potential, and promoted the expression of AdipoR1, p-LKB1, p-AMPKα, SIRT1, and PGC-1a in a cellular model of NAFLD. Further, silencing of AdipoR1 inhibited the ameliorative effect of YCLLT in the NAFLD cell model. Altogether, Yinchen lipid-lowering tea attenuates lipid deposition in a fatty liver model by improving mitochondrial function via activating AdipoR1/AMPK/ SIRT1 signaling.
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Registered trials
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