Article Sidebar
Published:
Jul 7, 2021Keywords:
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
Protective effect of valproic acid on MPP<sup>+</sup> -induced neurotoxicity in dopaminergic SH-SY5Y cells through Cdk5/p35/Erk signaling cascade
Abstract
Purpose: To investigate the neuroprotective effect of valproic acid (VPA) on 1-methyl-4- phenylpyridinium (MPP+)-induced dopaminergic cell loss in human neuroblastoma SH-SY5Y cells.
Methods: Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Reactive oxygen species (ROS) generation in MPP+-treated SH-SY5Y cells was investigated by DCFH-DA. Apoptotic cell death was confirmed by Hoechst 33342 staining. The protective effect of VPA via Cdk5 and p35 cascade was investigated by reverse transcription polymerase chain reaction (RT-PCR) and Western blot (WB) analysis. In addition, further investigation on cell survival was performed using Western blot analysis through Erk signaling pathway.
Results: Cell viability was dramatically decreased in cells treated with MPP+ in a concentrationdependent manner (p < 0.05). Pre-treatment with VPA ameliorated MPP+-induced death of dopaminergic cell via inhibition of ROS generation (p < 0.05). VPA restored Cdk5 and p35 expression and significantly increased cell survival mediated by Erk activity (pErk/Erk).
Conclusion: The results from this study confirmed that VPA attenuated MPP+-induced dopaminergic cell death by the inhibition of ROS production via Cdk5/p35 cascade and Erk signaling pathway. VPA is thus a potential therapeutic candidate for the treatment of dopaminergic cell death via Cdk5/p35 cascade.
