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Hydroxycitric acid ameliorates inlfammation and oxidative stress in mouse models of multiple sclerosis
Institution:1. Department of Physiology and Pharmacology, Faculty of Medicine, Alborz University of Medical Sciences, Karaj, Iran;2. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran;3. Department of Microbiology and Immunology, School of Medicine,Alborz University of Medical Sciences, Karaj, Iran;4. Research Centre for Immunodeifciencies, Pediatrics Centre of Excellence, Children’s Medical Centre, Tehran University of Medical Sciences, Tehran, Iran;5. Growth and Development Research Centre, Paediatrics Centre of Excellence, Children’s Medical Centre, Tehran University of Medical Sciences, Tehran, Iran;6. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran;7. Department of Laboratory Medicine, Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran
Abstract:Hydroxycitric acid (HCA) is derived primarily from the Garcinia plant and is widely used for its anti-in-lfammatory effects. Multiple sclerosis can cause an inlfammatory demyelination and axonal damage. In this study, to validate the hypothesis that HCA exhibits therapeutic effects on multiple sclerosis, we established female C57BL/6 mouse models of multiple sclerosis,i.e., experimental autoimmune encephalomyelitis, using Complete Freund’s Adjuvant (CFA) emulsion containing myelin oligodendrocyte glycoprotein (35–55). Treatment with HCA at 2 g/kg/d for 3 weeks obviously improved the symptoms of nerve injury of experimental autoimmune encephalomyelitis mice, decreased serum interleulin-6, tumor necrosis factor alpha, nitric oxide, and malondialdehyde levels, and increased superoxide dismutase and glutathione reduc-tase activities. hTese ifndings suggest that HCA exhibits neuroprotective effects on multiple sclerosis-caused nerve injury through ameliorating inlfammation and oxidative stress.
Keywords:nerve regeneration  hydroxycitric acid  multiple sclerosis  inlfammation  oxidative stress  experimental autoimmune encephalomyelitis  neural regeneration
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