Open AccessHydroxycitric acid ameliorates inflammation and oxidative stress in mouse models of multiple sclerosis
Author(s) -
Mahdi Goudarzvand,
Sanaz Afraei,
Somayeh Yaslianifard,
Saleh Ghiasy,
Ghazal Sadri,
Mustafa Kalvandi,
Tina Alinia,
Ali Mohebbi,
Reza Yazdani,
Shahin Khadem Azarian,
Abbas Mirshafiey,
Gholamreza Azizi
Publication year - 2016
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.193240
Subject(s) - experimental autoimmune encephalomyelitis , multiple sclerosis , oxidative stress , myelin oligodendrocyte glycoprotein , medicine , malondialdehyde , neuroprotection , superoxide dismutase , inflammation , pharmacology , encephalomyelitis , nitric oxide , immunology , endocrinology
Hydroxycitric acid (HCA) is derived primarily from the Garcinia plant and is widely used for its anti-inflammatory effects. Multiple sclerosis can cause an inflammatory 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 reductase activities. These findings suggest that HCA exhibits neuroprotective effects on multiple sclerosis-caused nerve injury through ameliorating inflammation and oxidative stress.