Unlocking Therapeutic Potential: Camphorquinone's Role in Alleviating Non-Alcoholic Fatty Liver Disease via SIRT1/LKB1/AMPK Pathway Activation.

BACKGROUND

Non-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.

METHODS

CQ (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.

RESULTS

CQ 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.

CONCLUSION

Collectively, 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.