title: Catechin hydrate ameliorates redox imbalance and limits inflammatory response in focal cerebral ischemia.
abstract: Epidemiologic studies have shown that foods rich in polyphenols, such as flavonoids, can lower the risk of ischemic disease; however, the mechanism of protection has not been clearly investigated. In this study, we hypothesized that pretreatment effect of catechin hydrate (CH) on functional outcome, neuronal damage and on secondary injuries in the ischemic brain of rats. To test this hypothesis, male Wistar rats were pretreated with CH (20 mg/kg b.wt) for 21 days and then subjected to 2 h middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion. After 2 h MCAO/22 h reperfusion, neurological deficit, infarct sizes, activities of antioxidant enzymes and cytokines level were measured. Immunohistochemistry and western blot were used to analyse the expression of glial fibrillary acidic protein (GFAP), inducible nitric oxide (iNOS) and NF-kB in ischemic brain. The administration of CH showed marked reduction in infarct size, reduced the neurological deficits, suppressed neuronal loss and downregulate the iNOS, GFAP and NF-kB expression in MCAO rats. A significantly depleted activity of antioxidant enzymes and content of glutathione in MCAO group were protected significantly in MCAO group pretreated with CH. Conversely, the elevated level of thiobarbituric acid reactive species and cytokines in MCAO group was attenuated significantly in CH pretreated group when compared with MCAO group. The results indicated that CH protected the brain from damage caused by MCAO, and this effect may be through downregulation of NF-kB expression.
authors.affiliation: Neurotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India.
authors.forename: Mohammad
authors.initials: M
authors.lastname: Ashafaq
authors.forename: Syed Shadab
authors.initials: SS
authors.lastname: Raza
authors.forename: Mohd Moshahid
authors.initials: MM
authors.lastname: Khan
authors.forename: Ajmal
authors.initials: A
authors.lastname: Ahmad
authors.forename: Hayate
authors.initials: H
authors.lastname: Javed
authors.forename: Md Ejaz
authors.initials: ME
authors.lastname: Ahmad
authors.forename: Rizwana
authors.initials: R
authors.lastname: Tabassum
authors.forename: Farah
authors.initials: F
authors.lastname: Islam
authors.forename: M Saeed
authors.initials: MS
authors.lastname: Siddiqui
authors.forename: Mohammed M
authors.initials: MM
authors.lastname: Safhi
authors.forename: Fakhrul
authors.initials: F
authors.lastname: Islam
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001522:Behavior, Animal / Q000187:drug effects; D001921:Brain / Q000187:drug effects; D002545:Brain Ischemia / Q000378:metabolism*; D002392:Catechin / Q000494:pharmacology*; D002544:Cerebral Infarction / Q000473:pathology / Q000517:prevention & control; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D005978:Glutathione / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000503:physiopathology; D008297:Male; D016328:NF-kappa B / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D010084:Oxidation-Reduction; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005904:Glial Fibrillary Acidic Protein; D016328:NF-kappa B; D017392:Thiobarbituric Acid Reactive Substances; D002392:Catechin; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D005978:Glutathione