title: Hesperidin ameliorates functional and histological outcome and reduces neuroinflammation in experimental stroke.
abstract: Incidence of stroke is considered to be a major cause of death throughout the world. The middle cerebral artery occlusion (MCAO) for 2h followed by 22h of reperfusion model was used in male Wistar rats to study the protection of stroke by hesperidin. Hesperidin administration (50mg/kg b.wt.) once daily for 15days has improved the infarct size, reduced the neurological deficits in terms of behaviors, and protected the elevated level of thiobarbituric acid reactive species (TBARS). A significantly depleted activity of antioxidant enzymes, glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) and content of glutathione (GSH) in MCAO group were protected significantly in MCAO group pretreated with hesperidin. Moreover, inflammatory mediators like TNF-α, IL-1β levels, expression of iNOS and glial fibrillary acidic protein (GFAP) were significantly attenuated in H+MCAO group as compared to MCAO group. In conclusion, prophylactic treatment with hesperidin ameliorated the functional and histological outcomes with elevated endogenous antioxidants status as well as reduced induction of proinflammatory cytokines in MCA occluded rat. We theorized that hesperidin is among the pharmacological agents that reduce free radicals and its associated inflammation and have been found to limit the extent of brain damage following stroke.
authors.affiliation: Neurotoxicology Laboratory, Department of Medical Elementology & Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India.
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: Mohammad
authors.initials: M
authors.lastname: Ashafaq
authors.forename: Gulrana
authors.initials: G
authors.lastname: Khuwaja
authors.forename: Rizwana
authors.initials: R
authors.lastname: Tabassum
authors.forename: Hayate
authors.initials: H
authors.lastname: Javed
authors.forename: Mohammad 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; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D020520:Brain Infarction / Q000209:etiology; D002374:Catalase / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004660:Encephalitis / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006569:Hesperidin / Q000494:pharmacology / Q000627:therapeutic use*; D020244:Infarction, Middle Cerebral Artery / Q000150:complications; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects; D053580:Muscle Strength / Q000187:drug effects; D052247:Nitric Oxide Synthase Type II; D011597:Psychomotor Performance / Q000187:drug effects; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D006569:Hesperidin; D002374:Catalase; D005979:Glutathione Peroxidase; D052247:Nitric Oxide Synthase Type II; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione