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Original Research Article | OPEN ACCESS

Eriodictyol modulates glioma cell autophagy and apoptosis by inhibition of PI3K/Akt/mTOR signaling pathway

Lang Zeng1, Wen Fan1, Liang Tao1, Song Cao2, Yuefei Wang1, Qin Tu1

1Department of Neurosurgery; 2Department of Intensive Care Unit, Tongren Hospital of Wuhan University (Wuhan Third Hospital), Wuhan, Hubei 430070, China.

For correspondence:-  Qin Tu   Email: dr.tuqin@yahoo.com   Tel:+86276539 9972

Accepted: 15 October 2020        Published: 30 November 2020

Citation: Zeng L, Fan W, Tao L, Cao S, Wang Y, Tu Q. Eriodictyol modulates glioma cell autophagy and apoptosis by inhibition of PI3K/Akt/mTOR signaling pathway. Trop J Pharm Res 2020; 19(11):2329-2336 doi: 10.4314/tjpr.v19i11.12

© 2020 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 effects of eriodictyol (ERD) on U251 human glioma cell cycle and viability, autophagy and apoptosis by modulation of PI3/Akt/mTOR signaling cascade.
Methods: 740 Y-P was used to activate U251 human glioma cells. For exploring ERD effects, the U251 cells were treated with ERD and 740 Y-P together. MTT assay was used to elucidate cell viability and apoptosis. The expression of autophagic proteins (LC3B and Beclin-1), and apoptotic proteins (Bcl-2 and Bax) were quantified using Western blotting. To explore the role of PI3K/Akt/mTOR signaling pathway, their expression was measured in comparison to their respective phosphorylated derivatives by Western blotting.
Results: ERD exposure downregulated p-PI3K and p-Akt protein expression. The results also indicate that ERD reduced cell viability and stimulated apoptosis in U251 cells (p < 0.05). Consequently, Bax expression was upregulated and the expression of Bcl-2 was downregulated. ERD enhanced the autophagy of glioma cells U251 by enhancing LC3B and Beclin-1 expression (p < 0.05). These effects were opposite to that revealed by 740 Y-P exposure alone.
Conclusion: ERD reduces U251 human glioma cell viability, and triggers cell autophagy and apoptosis, which is significantly correlated to downregulation of PI3K/Akt/mTOR signalling cascade. Thus, the compound can potentially be used for the treatment of glioma.

Keywords: Eriodictyol, Glioma, U251 human glioma cell, Apoptosis, Autophagy

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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