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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-9827
Vol. 15, No. 2, 2016, pp. 241-251
Bioline Code: pr16032
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 15, No. 2, 2016, pp. 241-251

 en Neuroprotective effects of Ellagic acid on Neonatal Hypoxic Brain Injury via Inhibition of Inflammatory Mediators and Down-regulation of JNK/p38 MAPK Activation
Chen, Si-Yan; Zheng, Kuang & Wang, Zhi-quan

Abstract

Purpose: To investigate if ellagic acid exerts neuroprotective effects in hypoxic-ischemic (HI) brain injury by inhibiting apoptosis and inflammatory responses.
Methods: Separate groups of rat pups from post-natal day 4 (D4) were administered with ellagic acid (10, 20 or 40 mg/kg body weight) orally till post-natal day 10 (D10). On D10, the rats were subjected to HI brain injury. Following HI injury, infarct size, weight and volume of the brain were measured. Apoptosis was assessed by Fluoro-Jade C staining. Expression of caspases (caspase-3, 8 and 9), apoptotic pathway proteins (Bax, Bad, Bcl-2 and Bcl-xL), MAPKs, NF-κB(p65) and p-IK-Bα were assessed by western blotting. mRNA levels of inflammatory mediators (TNF-α, IL-1α, IL-1β, iNOS, COX-2) were analyzed.
Results: Ellagic acidmarkedly (p < 0.05) reduced infarct size, volume and tissue loss. Significant (p < 0.05) reduction in neuroapoptosis was observed on pre-treatment with ellagic acid. Expression levels of caspases, apoptotic pathway proteins and MAPK proteins were down-regulated with marked (p < 0.05) suppression of inflammatory mediators, NF-κB(p65) and p-IK-Bα.
Conclusion: Ellagic acid affords neuroprotection in HI brain injury by inhibiting apoptosis, inflammatory responses and modulating the proteins of apoptotic and MAPK pathways. Thus, ellagic acid may be a potent candidate for the treatment of HI injury.

Keywords
Brain injury; Ellagic acid; Hypoxia; Inflammatory mediators; Mitogen-activated protein kinases; Neuroprotective

 
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