ArticleTissue engineering and regenerative medicine2025
Unlocking Therapeutic Potential: Camphorquinone's Role in Alleviating Non-Alcoholic Fatty Liver Disease via SIRT1/LKB1/AMPK Pathway Activation.
Article in Tissue engineering and regenerative medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The LKB1-AMPK pathway in NAFLD: molecular mechanisms and therapeutic implications.Journal of physiology and biochemistry · 2026Review
- Camphor alleviates renal fibrosis by suppressing oxidative stress and inflammation, up-regulating SIRT1 and down-regulating NF-κB and TGF-β.Molecular and cellular biochemistry · 2026Article
- Advanced 3D In Vitro Liver Fibrosis Models: Spheroids, Organoids, and Liver-on-Chips.Biomimetics (Basel, Switzerland) · 2025Review
- Natural products intervene in non-alcoholic fatty liver disease by regulating the AMPK signaling pathway: preclinical evidence and mechanism.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro.
methodsCQ (10 or 30 mg/kg/day; i.p.) was injected for three weeks, and fasting blood glucose levels, glucose tolerance, and liver lipid metabolism were assessed.
resultsCQ administration alleviated the increase in body and liver weights and improved glucose tolerance in NAFLD mice model. CQ also reduced the gene expression levels of lipid biosynthesis and inflammation markers, while increasing the levels of fatty acid oxidation markers in liver tissues and HepG2 cells. These beneficial effects of CQ were mediated via activation of the sirtuin 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) signalling pathway in vitro and in vivo.
conclusionCollectively, our data suggest that CQ improves liver lipid metabolism and reduces blood glucose levels via activation of the SIRT1/serine/threonine kinase 11 (STK11/LKB1)/AMPK axis.
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