Article Sidebar
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Eriodictyol modulates glioma cell autophagy and apoptosis by inhibition of PI3K/Akt/mTOR signaling pathway
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.
