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 % O 2 ) 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
Highlights
Hypoxic-ischemic encephalopathy (HIE) is a severe complication of peripartum asphyxia that can result in severe neurological sequelae or disabilities and is often fatal [1]
The present study explored the neuroprotective efficacy of Alpha-lipoic acid (ALA) against hypoxic– ischemic (HI) brain injury in neonatal rats, by evaluating cerebral infarct area, the degree of edema, and the levels of several important oxidative stress and inflammatory markers
In the two ALA treatment groups (50 and 100 mg/kg), the decreases in the infarct area compared to the HI group were significant (p < 0.01) (Figure 1C)
Summary
Hypoxic-ischemic encephalopathy (HIE) is a severe complication of peripartum asphyxia that can result in severe neurological sequelae or disabilities and is often fatal [1]. The present study explored the neuroprotective efficacy of ALA against hypoxic– ischemic (HI) brain injury in neonatal rats, by evaluating cerebral infarct area, the degree of edema, and the levels of several important oxidative stress and inflammatory markers. Male Sprague-Dawley rat pups (7 days old, P7), weighing 15–20 g were obtained from the Experimental Animal Center (Shaanxi, China). After a 1-h recovery period, the rats were placed for 2.5 h in a hypoxia chamber (8 % O2, 92 % N2) maintained at a temperature of 37 °C with the assistance of a water bath They were moved back to their respective dams and immediately injected intraperitoneally (i.p.) with saline in the control group and ALA in the ALA groups as a one-time post-treatment. One half of the brain was used for morphological analysis (infarct area) and the remaining half for biochemical and molecular analyses by homogenizing the cerebral region (pooled) in lysis buffer
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