Abstract

–Huntington’s disease (HD) is an autosomal dominant inherited neurodegenerative disease that causes clinical manifestations such as progressive choreiformic movements, cognitive abnormality and psychiatric deterioration. HD results from the destruction of neurons in the basal ganglia, and oxidative stress, Exitotoxicity and energy impairment hasbeen implicated in its pathogenesis. 3-Nitropropionic acid (3NP), a potent neurotoxin, has been reported to induce oxidative/ nitrosative stress and causes neurobehavioral and biochemical changes that mimic HD in humans. In the present work, we evaluated the effects of a well-known antioxidant on behavioral, biochemical, and mitochondrial dysfunction induced by 3NP. The study was designed to investigate the neuroprotective effects of Ethanolic extract of Zingiber oficinale against 3-NP-induced neurotoxicity. Intraperitoneal administration of 3-NP (20 mg/kg for 7 days) caused a decline in motor function (locomotor activity and impaired rotarod activity). Chronic treatment with EEZO root extracts (100 and 200 mg/kg) for 1 week dose-dependently improved 3-NP-induced behavioral, biochemical, and enzymatic changes (P < .05). Biochemical analysis revealed that systemic 3-NP administration significantly increased lipid peroxidation and nitrite and acetylcholiestrease level, Chronic administration of EEZO (100 and 200 mg/kg) dose-dependently restored biochemical alterations induced by chronic 3-NP treatment (P<.05). These findings suggest that neuroprotective actions of Zingiber officinale are mediated via its anticholinesterase activity. However, further studies are required to elucidate the molecular mechanisms involved in order to support the clinical use of the plant extract as a therapeutic agent for the treatment of HD. Keywords––Huntington’s disease, oxidative stress, Zingiber officinale, Neuroprotective, 3-nitropropionic

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