Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Quercetin promotes MC3T3-E1 cell growth via PI3K/Akt signaling pathway

Haidong Liang , Fang Yu

Dalian Medical University, Dalian City, China;

For correspondence:- Haidong Liang Email: tsfkmei@aliyun.com Tel:+8641184671291

Accepted: 21 November 2018 Published: 26 December 2018

Citation: Liang H, Yu F. Quercetin promotes MC3T3-E1 cell growth via PI3K/Akt signaling pathway. Trop J Pharm Res 2018; 17(12):2371-2374 doi: 10.4314/tjpr.v17i12.8

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of quercetin on mouse osteoblast MC3T3-E1 cell growth and the molecular mechanisms involved.

Methods: The effect of quercetin on MC3T3-E1 cells growth, cell cycle distribution, bone-related genes and PI3K/Akt signaling pathway were determined in vitro using MTT assay, flow cytometry, qPCR and western blot, respectively.

Results: Qercetin promoted MC3T3-E1 cell growth, as revealed from MTT assay. Flow cytometry showed that quercetin administration resulted in accumulation of cells in the S phase. In addition, quercetin up-regulated mRNA expression levels of osteopontin, ALP, osteoprotegerin, osteocalcin and RunX-2, and increased phosphorylation of AKT.

Conclusion: Quercetin enhances the growth of MC3T3-E1 cells via a mechanism involving accumulation of cells in S phase, increasing mRNA expression levels of bone-associated genes, and increasing the phosphorylation of AKT.

Keywords: Quercetin, MC3T3-E1 cells, AKT phosphorylation, Osteopontin, Osteoprotegerin, Osteocalcin, RunX-2