Neuroprotective effect of punicalagin against cerebral ischemia reperfusion-induced oxidative brain injury in rats
| Autor: | Bavya Byna, Santh Rani Thakur, Lavanya Yaidikar |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Time Factors Glutathione reductase Ischemia Brain Edema Pharmacology medicine.disease_cause Antioxidants Superoxide dismutase Brain ischemia Protein Carbonylation chemistry.chemical_compound medicine Animals Rats Wistar chemistry.chemical_classification biology business.industry Glutathione peroxidase Rehabilitation Brain Infarction Middle Cerebral Artery Glutathione medicine.disease Malondialdehyde Hydrolyzable Tannins Mitochondria Disease Models Animal Oxidative Stress Neuroprotective Agents chemistry Anesthesia Reperfusion Injury biology.protein Surgery Neurology (clinical) Cardiology and Cardiovascular Medicine business Oxidative stress Biomarkers |
| Zdroj: | Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association. 23(10) |
| ISSN: | 1532-8511 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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