title: S-allyl cysteine mitigates oxidative damage and improves neurologic deficit in a rat model of focal cerebral ischemia.
abstract: Oxidative stress and inflammatory damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The present study examined the hypothesis that S-allyl cysteine (SAC), organosulfur compounds found in garlic extract, would reduce oxidative stress-associated brain injury after middle cerebral artery occlusion (MCAO). To test this hypothesis, male Wistar rats were subjected to MCAO for 2 hours and 22-hour reperfusion. S-allyl cysteine was administered (100 mg/kg, b.wt.) intraperitoneally 30 minutes before the onset of ischemia and after the ischemia at the interval of 0, 6, and 12 hours. After 24 hours of reperfusion, rats were tested for neurobehavioral activities and were killed for the infarct volume, estimation of lipid peroxidation, glutathione content, and activity of antioxidant enzymes (glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase). S-allyl cysteine treatment significantly reduced ischemic lesion volume, improved neurologic deficits, combated oxidative loads, and suppressed neuronal loss. Behavioral and biochemical alterations observed after MCAO were further associated with an increase in glial fibrillary acidic protein and inducible nitric oxide expression and were markedly inhibited by the treatment with SAC. The results suggest that SAC exhibits exuberant neuroprotective potential in rat ischemia/reperfusion model. Thus, this finding of SAC-induced adaptation to ischemic stress and inflammation could suggest a novel avenue for clinical intervention during ischemia and reperfusion.
authors.affiliation: Department of Medical Elementology and Toxicology (Fund for the Improvement of Science and Technology sponsored by DST and Special Assistance Programme sponsored by UGC), JamiaHamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India.
authors.forename: Mohammad
authors.initials: M
authors.lastname: Ashafaq
authors.forename: Mohd Moshahid
authors.initials: MM
authors.lastname: Khan
authors.forename: Syed
authors.initials: S
authors.lastname: Shadab Raza
authors.forename: Ajmal
authors.initials: A
authors.lastname: Ahmad
authors.forename: Gulrana
authors.initials: G
authors.lastname: Khuwaja
authors.forename: Hayate
authors.initials: H
authors.lastname: Javed
authors.forename: Andleeb
authors.initials: A
authors.lastname: Khan
authors.forename: Farah
authors.initials: F
authors.lastname: Islam
authors.forename: M 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: D000490:Allium / Q000737:chemistry*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001522:Behavior, Animal / Q000187:drug effects; D002545:Brain Ischemia / Q000188:drug therapy*; D054022:Cerebrum / Q000187:drug effects; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000517:prevention & control; D007249:Inflammation / Q000188:drug therapy; D008297:Male; D009422:Nervous System Diseases / Q000188:drug therapy; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control*
chemical_list: D000975:Antioxidants; D005904:Glial Fibrillary Acidic Protein; D018696:Neuroprotective Agents; D010936:Plant Extracts; D009569:Nitric Oxide; C065299:S-allylcysteine; D003545:Cysteine