Article Sidebar
Published:
Jun 2, 2017Keywords:
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 effects of α-lipoic acid against hypoxic– ischemic brain injury in neonatal rats
Abstract
Purpose: To explore the neuroprotective efficacy of α-lipoic acid (ALA) against hypoxic-ischemic encephalopathy (HIE) in neonatal rats.
Methods: Forty-eight rats (P7-pups) were randomly assigned to one of four groups: group I received saline; group II (HI) underwent unilateral carotid artery ligation and hypoxia (92 % N2 and 8 % O2) for 2.5 h; and groups III and IV (ALA 50 and 100) were treated with 50 or 100 mg ALA/kg for 7 days prior to against hypoxic-ischemic (HI) insult. Cerebral antioxidant status, edema, and the levels of inflammatory markers were determined.
Results: ALA administration substantially (p < 0.01) attenuated both cerebral infarct area and degree of edema while decreasing the levels of several inflammatory markers (TNF-α, NF-p65, IL-1β, IL-6). In addition, in the ALA groups, antioxidant enzyme (SOD, CAT, GSH) activities were significantly elevated,
while the expressions of TNF-α and IL-1β protein were significantly (p < 0.01) down-regulated.
Conclusion: The neuroprotective efficacy of ALA in HIE can be attributed to its suppression of both oxidative stress and the levels of inflammatory markers.
Keywords: Hypoxic–ischemic brain injury, α-Lipoic acid, Cerebral infarct area, Edema, Antioxidants, Inflammatory markers
