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Neuroprotective potential of escitalopram against behavioral, mitochondrial and oxidative dysfunction induced by
Shruthi Shetty1, Ashwini Hariharan1, Trupti Shirole1
1Department of Pharmacology, Bombay College of Pharmacy, Kalina, Santacruz East, Mumbai 400 098, India.
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.
