S-allyl cysteine mitigates oxidative damage and improves neurologic deficit in a rat model of focal cerebral ischemia |
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Authors: | Mohammad Ashafaq Mohd. Moshahid Khan Syed Shadab Raza Ajmal Ahmad Gulrana Khuwaja Hayate Javed Andleeb Khan Farah Islam M. Saeed Siddiqui Mohammed M. Safhi Fakhrul Islam |
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Affiliation: | 1. Neurotoxicology laboratory, 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;2. Department of Neurology, Carver College of Medicine, University of Iowa, IA, USA;3. Department of Neurology, Georgia Health Sciences University, Augusta, GA 30912, USA;4. Department of Biotechnology, Faculty of Pharmacy, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India;5. Neuroscience and Toxicology Unit, College of Pharmacy, Jazan University, Jazan, Kingdom of Saudi Arabia |
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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. |
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Keywords: | DAB, diaminobenzidine EDTA, ethylenediamine tetra acetic acid EGTA, ethylene glycol tetraacetic acid GFAP, glial fibrillary acidic protein GPx, glutathione peroxidase GR, glutathione reductase GSH, reduced glutathione CAT, catalase iNOS, inducible nitric oxide synthase LPO, lipid peroxidation MCAO, middle cerebral artery occlusion NADPH, nicotinamide adenine dinucleotide phosphate PB, phosphate buffer PBS, phosphate buffer saline PMS, postmitochondrial supernatant ROS, reactive oxygen species SAC, S-allyl cysteine SOD, superoxide dismutase TBARS, thiobarbituric acid reactive substances TTC, 2,3,5-triphenyltetrazolium chloride |
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