Neuroprotective potential of escitalopram against behavioral, mitochondrial and oxidative dysfunction induced by 3-nitropropionic acid

摘要

Background: Huntington’s disease (HD) is a neurodegenerative disorder characterized by cognitive dysfunction and abnormal body movements called chorea.There exists no therapeutic agent to address the disease.3-Nitropropionic acid (3-NP) is a well-known experimental model to study Huntington’s disease. It is a suicide inhibitor of succinate dehydrogenase and causes gait and memory impairment which leads to oxidative and neuronal damage. Purpose: In the present study the protective effect of escitalopram against 3-NP induced neurotoxicity was explored. Methods: Adult female Wistar ratswere subjected to per oral administration of 2 different doses of escitalopram (10 and 20mg/kg) for 12 days followed by intraperitoneal injection of 3-NP (20mg/kg) on the last four days. Results: Systemic administration of 3-NP significantly induced HD like symptoms in rats such as impaired memory, decreased locomotor activity, hind limb impairment, decreased body weight, oxidative damage and mitochondrial dysfunction. Treatment with 2 different dose of escitalopram significantly reversed behavioural, biochemical and mitochondrial enzyme dysfunctions induced by 3-NP. Further, histopathological examination confirmed the neuroprotective effect of escitalopram against 3-NP induced pathological lesions. Conclusion: The results obtained thus suggests the possible antioxidant and neuroprotective role of escitalopram against 3-NP induced alterations in rats thereby indicating that it can be a promising candidate for the management of HD.