Article Sidebar
Published:
Sep 5, 2016Keywords:
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
Neuroprotective effect of apocynin nitrone in oxygen glucose deprivation-treated SH-SY5Y cells and rats with ischemic stroke
Abstract
Purpose: To investigate the neuroprotective potential of apocynin nitrone (AN-1), a nitrone analogue of apocynin, in rat brain tissue as a novel candidate for ischemic stroke treatment.
Methods: In vitro neuroprotection of AN-1 was studied in SH-SY5Y cells treated with oxygen glucose deprivation (OGD). Cell viability was measured using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2Htetrazolium bromide (MTT) assay, and intracellular reactive oxygen species (ROS) level was investigated using flow cytometry. The protection of AN-1 in cerebral ischemia-reperfusion (I/R) rats was evaluated by cerebral infarct area and neurological deficit score. Oxidative stress of the ischemic hemisphere was assessed by malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) levels.
Results: In OGD-treated SH-SY5Y cells, AN-1 reduced cell death and ROS level. In I/R rats, AN-1 exerted potential protection against neurological deficit by reducing infarction area, decreasing neurological deficit score and relieving oxidative stress. AN-1 exhibited stronger action than its parent compound apocynin in vitro, but the two had similar effects in vivo. In addition, AN-1 demonstrated efficacy close to or higher than the positive reference Edaravone® both in vitro and in vivo.
Furthermore, AN-1 showed lower toxicity than apocynin in vitro.
Conclusion: The results suggest that AN-1 may be a potential neuroprotective agent for the treatment of ischemic stroke in human.
Keywords: Apocynin nitrone, Cerebral ischemia-reperfusion injury, Neuroprotection, Reactive oxygen species, Oxidative stress
