title: Sesamin attenuates behavioral, biochemical and histological alterations induced by reversible middle cerebral artery occlusion in the rats.
abstract: Restoration of blood flow to an ischemic brain region is associated with generation of reactive oxygen species (ROS) with consequent reperfusion injury. ROS cause lipid peroxidation, protein oxidation, and DNA damage, all of which are deleterious to cells. So diminishing the production of free radicals and scavenging them may be a successful therapeutic strategy for the protection of brain tissue in cerebral stroke. The present study investigated the neuroprotective effect of sesamin (Sn) to reduce brain injury after middle cerebral artery occlusion (MCAO). The middle cerebral artery (MCA) of adult male Wistar rat was occluded for 2h and reperfused for 22h. Sesamin is the most abundant lignan in sesame seed oil is a potent antioxidant. Sesamin (30 mg/kg) was given orally twice, 30 min before the onset of ischemia and 12h after reperfusion. The initial investigations revealed that sesamin reduced the neurological deficits in terms of behavior and reduced the level of thiobarbituric acid reactive species (TBARS), and protein carbonyl (PC) in the different areas of the brain when compared with the MCAO group. A significantly depleted level of glutathione and its dependent enzymes (glutathione peroxidase [GPx] and glutathione reductase [GR]) in MCAO group were protected significantly in MCAO group treated with sesamin. The present study suggests that sesamin may be able to attenuate the ischemic cell death and plays a crucial role as a neuroprotectant in regulating levels of reactive oxygen species in the rat brain. Thus, sesamin may be a potential compound in stroke therapy.
authors.affiliation: Neurotoxicology Laboratory, Department of Medical Elementology & Toxicology (Fund for the Improvement of Science and Technology sponsored by DST and Special Assistance Programme sponsored by UGC), Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India. mushahidkhn@yahoo.co.in
authors.forename: Mohd Moshahid
authors.initials: MM
authors.lastname: Khan
authors.forename: Tauheed
authors.initials: T
authors.lastname: Ishrat
authors.forename: Ajmal
authors.initials: A
authors.lastname: Ahmad
authors.forename: Md Nasrul
authors.initials: MN
authors.lastname: Hoda
authors.forename: M Badruzzaman
authors.initials: MB
authors.lastname: Khan
authors.forename: Gulrana
authors.initials: G
authors.lastname: Khuwaja
authors.forename: Pallavi
authors.initials: P
authors.lastname: Srivastava
authors.forename: Syed Shadab
authors.initials: SS
authors.lastname: Raza
authors.forename: Fakhrul
authors.initials: F
authors.lastname: Islam
authors.forename: Saif
authors.initials: S
authors.lastname: Ahmad
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D004149:Dioxoles / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D017705:Lignans / Q000494:pharmacology*; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D004149:Dioxoles; D017705:Lignans; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D000254:Sodium-Potassium-Exchanging ATPase; D005978:Glutathione; C054125:sesamin