Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Neuroprotective effects of α-lipoic acid against hypoxic-ischemic brain injury in neonatal rats

Xiao-han Mei , You-wen Yang

Department of Pediatrics, Xianyang City Center Hospital of Shaanxi Province, Shaanxi 712000, China;

For correspondence:- Xiao-han Mei Email: meixiaohanxh@hotmail.com Tel:+862933222222

Received: 19 February 2017 Accepted: 13 April 2017 Published: 30 May 2017

Citation: Mei X, Yang Y. Neuroprotective effects of α-lipoic acid against hypoxic-ischemic brain injury in neonatal rats. Trop J Pharm Res 2017; 16(5):1051-1058 doi: 10.4314/tjpr.v16i5.12

© 2017 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 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: Hypoxicâ€“ischemic brain injury, ^5;-Lipoic acid, Cerebral infarct area, Edema, Antioxidants, Inflammatory markers