title: Hesperidin attenuates oxidative and neuronal damage caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model.
abstract: The aim of this study was to determine the effects of hesperidin (HP) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. For this purpose, a total of 40 mice were divided equally into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) HP, and (4) HP+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with vehicle for 10 days. In the HP group, mice were administered HP (100 mg/kg) for 10 days without carotid occlusion. In the HP+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with 100 mg/kg HP for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidation and a decrease in the components of the antioxidant defense system. Furthermore, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue. HP treatment significantly reversed the oxidative effects of I/R and inhibited the development of neurodegenerative histopathology. Therefore, the current study demonstrates that HP treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, the beneficial effects of HP are likely a result of its strong antioxidant and free radical-scavenging properties. HP may be an useful treatment to attenuate the negative effects of global cerebral I/R.
authors.affiliation: Department of Brain and Neurosurgery, Faculty of Medicine, University of Inonu, 44280, Malatya, Turkey, osmciftci@gmail.com.
authors.forename: M Namik
authors.initials: MN
authors.lastname: Oztanir
authors.forename: Osman
authors.initials: O
authors.lastname: Ciftci
authors.forename: Aslı
authors.initials: A
authors.lastname: Cetin
authors.forename: M Arif
authors.initials: MA
authors.lastname: Aladag
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy*; D053148:Caspase 3 / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007211:Indoles / Q000494:pharmacology / Q000627:therapeutic use*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects*; D015427:Reperfusion Injury; D013449:Sulfonamides / Q000494:pharmacology / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D007211:Indoles; D018696:Neuroprotective Agents; D013449:Sulfonamides; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D053148:Caspase 3; D005978:Glutathione; C474723:hesperadin