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

Authors :
Bhrigu Kumar Das
Rachel M. Knott
Pramod C. Gadad
Source :
Future Journal of Pharmaceutical Sciences, Vol 7, Iss 1, Pp 1-10 (2021)
Publication Year :
2021
Publisher :
SpringerOpen, 2021.

Abstract

Abstract Background Metabolic dysregulation is one of the hallmarks of tumor cell proliferation. Evidence indicates the potential role of the 5′adenosine monophosphate-activated protein kinase (AMPK) and protein kinase B/Akt signaling pathway in regulating cell proliferation, survival, and apoptosis. The present study explores the effect of metformin HCl and the combination of α- and β-asarone on the proliferation of HepG2 cells in the presence of high glucose levels simulating the diabetic-hepatocellular carcinoma (HCC) condition. Results The metformin and asarone reduced HepG2 cell viability in a dose-dependent manner and induced morphological changes as indicated by methyl thiazolyl tetrazolium (MTT) assay. The metformin and asarone arrested the cells at the G0/G1 phase, upregulated the expression of AMPK, and downregulated Akt expression in high glucose conditions as identified by the flow cytometry technique. Further, the upregulated AMPK led to a decrease in the expression of phosphoenolpyruvate carboxykinase-2 (PCK-2) and sterol regulatory element-binding protein-1 (SREBP-1). Conclusion The anti-proliferative effect of metformin and asarone in the diabetic-HCC condition is mediated via AMPK and Akt pathway.

Details

Language :
English
ISSN :
23147253
Volume :
7
Issue :
1
Database :
Directory of Open Access Journals
Journal :
Future Journal of Pharmaceutical Sciences
Publication Type :
Academic Journal
Accession number :
edsdoj.3affe6eaf6ba4756ba3323fc7e3eb9d8
Document Type :
article
Full Text :
https://doi.org/10.1186/s43094-021-00193-8