PMID- 19835851 OWN - NLM STAT- MEDLINE DCOM- 20100128 LR - 20220321 IS - 1872-7786 (Electronic) IS - 0009-2797 (Linking) VI - 183 IP - 1 DP - 2010 Jan 5 TI - Sesamin attenuates behavioral, biochemical and histological alterations induced by reversible middle cerebral artery occlusion in the rats. PG - 255-63 LID - 10.1016/j.cbi.2009.10.003 [doi] AB - 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. FAU - Khan, Mohd Moshahid AU - Khan MM AD - 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 FAU - Ishrat, Tauheed AU - Ishrat T FAU - Ahmad, Ajmal AU - Ahmad A FAU - Hoda, Md Nasrul AU - Hoda MN FAU - Khan, M Badruzzaman AU - Khan MB FAU - Khuwaja, Gulrana AU - Khuwaja G FAU - Srivastava, Pallavi AU - Srivastava P FAU - Raza, Syed Shadab AU - Raza SS FAU - Islam, Fakhrul AU - Islam F FAU - Ahmad, Saif AU - Ahmad S LA - eng PT - Journal Article PL - Ireland TA - Chem Biol Interact JT - Chemico-biological interactions JID - 0227276 RN - 0 (Antioxidants) RN - 0 (Dioxoles) RN - 0 (Lignans) RN - 0 (Neuroprotective Agents) RN - 0 (Reactive Oxygen Species) RN - 0 (Thiobarbituric Acid Reactive Substances) RN - EC 1.11.1.9 (Glutathione Peroxidase) RN - EC 1.8.1.7 (Glutathione Reductase) RN - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase) RN - GAN16C9B8O (Glutathione) RN - S7946O4P76 (sesamin) SB - IM MH - Animals MH - Antioxidants/*pharmacology MH - Behavior, Animal/drug effects MH - Dioxoles/*pharmacology MH - Glutathione/metabolism MH - Glutathione Peroxidase/metabolism MH - Glutathione Reductase/metabolism MH - Infarction, Middle Cerebral Artery/drug therapy/*metabolism/pathology MH - Lignans/*pharmacology MH - Male MH - Motor Activity/drug effects MH - Neuroprotective Agents/*pharmacology MH - Protein Carbonylation MH - Rats MH - Rats, Wistar MH - Reactive Oxygen Species/metabolism MH - Sodium-Potassium-Exchanging ATPase/metabolism MH - Thiobarbituric Acid Reactive Substances/metabolism EDAT- 2009/10/20 06:00 MHDA- 2010/01/29 06:00 CRDT- 2009/10/20 06:00 PHST- 2009/07/05 00:00 [received] PHST- 2009/10/01 00:00 [revised] PHST- 2009/10/07 00:00 [accepted] PHST- 2009/10/20 06:00 [entrez] PHST- 2009/10/20 06:00 [pubmed] PHST- 2010/01/29 06:00 [medline] AID - S0009-2797(09)00432-3 [pii] AID - 10.1016/j.cbi.2009.10.003 [doi] PST - ppublish SO - Chem Biol Interact. 2010 Jan 5;183(1):255-63. doi: 10.1016/j.cbi.2009.10.003.