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

Abstract

BACKGROUND:

Huntington's disease (HD) is a neurodegenerative syndrome that leads to marked decline in cognitive functioning along with uncharacteristic body movements called chorea. There exists no therapeutic agent to address the disease.3-Nitropropionic acid (3-NP) which is a suicide inhibitor of succinate dehydrogenase and a well-known experimental model to study Huntington's disease, causes substantial impairment in gait and memory through oxidative and neuronal damage.

PURPOSE:

In the present study 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 20 mg/kg) for 12 days followed by intraperitoneal injection of 3-NP (20 mg/kg) on the last four days.

RESULTS:

Intraperitoneal injection of 3-NP lead to significant induction of HD like symptoms in rats such as impaired memory, reduced locomotor activity, hind limb impairment, decreased body weight, oxidative damage and mitochondrial dysfunction. Treatment with 2 different dose of escitalopram helped reverse the mitochondrial enzyme dysfunction along with reversal of behavioural and biochemical anomaly induced by 3-NP. Further, histopathological examination confirmed the neuroprotective potential of escitalopram against 3-NP induced pathological lesions.

CONCLUSION:

The results obtained thus substantiate the claim that escitalopram might play an antioxidant and neuroprotective role against 3-NP induced alterations in rats and can prove to be a promising candidate for the management of HD.

• Authors: Shruthi Shetty, Ashwini Hariharan, Trupti Shirole, Aarti G Jagtap
• Journal: Annals of neurosciences (Ann Neurosci) Vol. 22 Issue 1 Pg. 11-8 (Jan 2015) ISSN: 0972-7531 [Print] United States
• PMID: 26124545 (Publication Type: Journal Article)