title: Quercetin protects against oxidative stress associated damages in a rat model of transient focal cerebral ischemia and reperfusion.
abstract: Experimental studies have demonstrated that oxidative stress and apoptosis play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The purpose of this study was to determine whether the quercetin dihydrate (Q) protects against cerebral ischemia neuronal damage. Male Wistar rats were subjected to transient middle cerebral artery occlusion (MCAO) for 2 h and reperfused for 72 h. Quercetin (30 mg/kg, i.p) was administrated 30 min before the onset of ischemia and after the ischemia at interval of 0, 24, 48, and 72 h. The administration of Q showed marked reduction in infarct size, reduced the neurological deficits in terms of behaviors, suppressed neuronal loss and diminished the p53 expression in MCAO rats. Q was found to be successful in upregulating the antioxidant status and lowering the TBARS level. Conversely, the elevated activity of poly (ADP-ribose) polymerase (PARP), and activity of caspase-3 in MCAO group was attenuated significantly in Q treated group when compared with MCAO group. Our study reveals that Q, as a powerful antioxidant, could prevent free radicals associated oxidative damage and morphological changes in the MCAO rats. Thus, it may have a therapeutic value for the treatment of stroke.
authors.affiliation: Neurotoxicology Laboratory, Department of Medical Elementology & Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, 110062, India.
authors.forename: Ajmal
authors.initials: A
authors.lastname: Ahmad
authors.forename: Mohd Moshahid
authors.initials: MM
authors.lastname: Khan
authors.forename: Md Nasrul
authors.initials: MN
authors.lastname: Hoda
authors.forename: Syed Shadab
authors.initials: SS
authors.lastname: Raza
authors.forename: M Badruzzaman
authors.initials: MB
authors.lastname: Khan
authors.forename: Hayate
authors.initials: H
authors.lastname: Javed
authors.forename: Tauheed
authors.initials: T
authors.lastname: Ishrat
authors.forename: Mohammad
authors.initials: M
authors.lastname: Ashafaq
authors.forename: Md Ejaz
authors.initials: ME
authors.lastname: Ahmad
authors.forename: Mohammed M
authors.initials: MM
authors.lastname: Safhi
authors.forename: Fakhrul
authors.initials: F
authors.lastname: Islam
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000473:pathology*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D011794:Quercetin / Q000494:pharmacology* / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control*; D045442:Rotarod Performance Test; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D016159:Tumor Suppressor Protein p53; D011794:Quercetin; D011065:Poly(ADP-ribose) Polymerases; D005978:Glutathione