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

Abstract

BackgroundHuntington’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.PurposeIn the present study protective effect of escitalopram against 3-NP induced neurotoxicity was explored.MethodsAdult 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.ResultsIntraperitoneal 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.ConclusionThe 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.

Brain cytochrome‐c‐oxidase as a marker of mitochondrial function: A pilot study in major depression using NIRS

“…The sample size was small and the MDE groups were heterogenous with respect to diagnosis, age, and medication status. Escitalopram has not been shown to affect mitochondrial function in general or COX activity in particular (Gonçalves et al, 2012;Shetty, Hariharan, Shirole, & Jagtap, 2015), although other SSRIs may decrease mitochondrial function (Adzic, Brkic, Bulajic, Mitic, & Radojcic, 2016;Hroudová & Fisar, 2010). LLD differs from younger patients with MDD in both pathophysiology and clinical presentation (Glover & Srinivasan, 2013).…”

“…We note that this patient's data were not outliers in the analysis. Escitalopram has not been shown to affect mitochondrial function in general or COX activity in particular (Gonçalves et al, 2012;Shetty, Hariharan, Shirole, & Jagtap, 2015), although other SSRIs may decrease mitochondrial function (Adzic, Brkic, Bulajic, Mitic, & Radojcic, 2016;Hroudová & Fisar, 2010). Further, 5/6 of patients with BD had commenced antidepressant treatment with fluoxetine, another SSRI, within 2 weeks of scanning.…”

Oxidative Stress Assessment in Alzheimer’s Disease: A Clinic Setting Study

“…34,50,51 We did not evaluate use of antidepressants for which a possible antioxidant effect was recently reported. [52][53][54] The result of lower OS in patients with AD having stable antidementia treatments we found should be interpreted with caution, as OS levels were not assessed in these patients before antidementia therapy.…”

“…34,50,51 We did not evaluate use of antidepressants for which a possible antioxidant effect was recently reported. 52 -54…”

Jobelyn® Supplement Lowered Neuronal Degeneration: Significance of Altered p53 and ɤ-Enolase Protein Expressions in Prefrontal Cortex of Rat Exposed to Ethanol

“…To answer the question whether the neuroprotective effect of Jobelyn is related to its antioxidative property, we estimated the MDA level in samples of the PFC. It is well known that an increased tissue level of MDA is directly proportional to the degree of LP and hence the extent of damage [40,41] . This study shows that Jobelyn significantly reduced the level of MDA in the tissue.…”