Neuroprotective Effect of Punicalagin against Cerebral Ischemia Reperfusion-induced Oxidative Brain Injury in Rats

• Published in: Journal of stroke and cerebrovascular diseases 2014-11, Vol.23 (10), p.2869-2878
• Main Authors: Yaidikar, Lavanya, MPharm, Byna, Bavya, MPharm, Thakur, Santh Rani, PhD
• Format: Article
• Language: English
• Subjects: Animals; antioxidant; Antioxidants - pharmacology; Biomarkers - metabolism; Brain - blood supply; Brain - drug effects; Brain - metabolism; Brain - pathology; Brain Edema - prevention & control; Cardiovascular; Cerebral ischemia/reperfusion injury; Disease Models, Animal; Hydrolyzable Tannins - pharmacology; Infarction, Middle Cerebral Artery - metabolism; Infarction, Middle Cerebral Artery - pathology; Infarction, Middle Cerebral Artery - prevention & control; Male; Mitochondria - drug effects; Mitochondria - metabolism; Neurology; Neuroprotective Agents - pharmacology; oxidative stress; Oxidative Stress - drug effects; Protein Carbonylation; punicalagin; Rats, Wistar; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Reperfusion Injury - prevention & control; Time Factors
• ISSN: 1052-3057; 1532-8511
• DOI: 10.1016/j.jstrokecerebrovasdis.2014.07.020

Background Punicalagin (PG) is a hydrolyzable polyphenol in Punica granatum . It has been previously reported that it has a protective effect against hypoxia-induced ischemia brain injury. It is a potent antioxidant. The present study is aimed to evaluate the antioxidant potential of PG against focal cerebral ischemia–reperfusion injury in rats subjected to middle cerebral artery occlusion (MCAO). Methods Rats were randomly divided into sham, MCAO, PG-treated groups. PG (15 and 30 mg/kg) vehicle was administered orally for 7 days before MCAO. Rats were anesthetized with ketamine (100 mg/kg), xylazine (10 mg/kg), and subjected to 2 hours occlusion, and 22 hours reperfusion. Neurologic deficit, brain water content (BWC), histopathology changes, and oxidative stress markers were evaluated after 22 hours of reperfusion. In comparison with MCAO model group, treatment with PG significantly reduced the neurologic deficit scores and BWC. Results PG-attenuated neuronal damage occurred by downregulating the levels of malondialdehyde, sodium–potassium adenosine triphosphatase activity, nitric oxide, protein carbonyl content, and mitochondria-generated reactive oxygen species and upregulating the superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, glutathione reductase activities. Conclusions Taken together, these results suggested that supplementation of PG treatment effectively ameliorates the cerebral ischemia/reperfusion induced oxidative damage by virtue of its antioxidant potential.