Quercetin Protects Against Oxidative Stress Associated Damages in a Rat Model of Transient Focal Cerebral Ischemia and Reperfusion

• Published in: Neurochemical research Vol. 36; no. 8; pp. 1360 - 1371
• Main Authors: Ahmad, Ajmal, Khan, Mohd. Moshahid, Hoda, Md. Nasrul, Raza, Syed Shadab, Khan, M. Badruzzaman, Javed, Hayate, Ishrat, Tauheed, Ashafaq, Mohammad, Ahmad, Md. Ejaz, Safhi, Mohammed M., Islam, Fakhrul
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.08.2011; Springer Nature B.V
• Subjects: Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Glutathione - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Hippocampus - pathology; Infarction, Middle Cerebral Artery - drug therapy; Infarction, Middle Cerebral Artery - pathology; Ischemic Attack, Transient - drug therapy; Ischemic Attack, Transient - pathology; Male; Neurochemistry; Neurology; Neurosciences; Original Paper; Oxidative Stress - drug effects; Poly(ADP-ribose) Polymerases - metabolism; Quercetin - pharmacology; Quercetin - therapeutic use; Rats; Rats, Wistar; Reperfusion Injury - prevention & control; Rotarod Performance Test; Thiobarbituric Acid Reactive Substances - metabolism; Tumor Suppressor Protein p53 - metabolism; Oxidative stress; Neuroprotection; Infarction; Quercetin dihydrate; Neurobehavioral; Middle cerebral artery occlusion
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-011-0458-6

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.