Metformin and asarone inhibit HepG2 cell proliferation in a high glucose environment by regulating AMPK and Akt signaling pathway

Abstract Background Metabolic dysregulation is one of the hallmarks tumor cell proliferation. Evidence indicates potential role 5′adenosine monophosphate-activated protein kinase (AMPK) and B/Akt signaling pathway in regulating proliferation, survival, apoptosis. The present study explores effect metformin HCl combination α- β-asarone on proliferation HepG2 cells presence high glucose levels simulating diabetic-hepatocellular carcinoma (HCC) condition. Results asarone reduced viability a dose-dependent manner induced morphological changes as indicated by methyl thiazolyl tetrazolium (MTT) assay. arrested at G 0 /G 1 phase, upregulated expression AMPK, downregulated Akt conditions identified flow cytometry technique. Further, AMPK led to decrease phosphoenolpyruvate carboxykinase-2 (PCK-2) sterol regulatory element-binding protein-1 (SREBP-1). Conclusion anti-proliferative diabetic-HCC condition mediated via pathway.