International Journal of Endorsing Health Science Research (Dec 2020)

Curcumin attenuates sensorimotor deficits induced by selective neuronal loss: A study in middle cerebral artery occlusionrat model of transient ischemic stroke.

  • Mufzala Shamim,
  • Nazish Iqbal Khan

DOI
https://doi.org/10.29052/IJEHSR.v8.i4.2020.212-222
Journal volume & issue
Vol. 8, no. 4
pp. 212 – 222

Abstract

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Background:Ischemic stroke is the most prevalent and major pathological stroke type.Increased systemic oxidative stressis a crucialunderlyingpathophysiological mechanismof ischemic stroke.In this regard, therapeutic interventions targeting oxidative stress management would be a promising avenue. Curcumin is well recognized to counteract various pathologieseffectively.The present study was designed to investigate the neuroprotective effects of curcumin against ischemia-reperfusion injury-induced selective neuronal damage. Methodology:Present study employed an ischemic brain injury model induced by middle cerebral artery occlusion (MCAO) inWistar albino rats. Experimental groups (n=36; age-matched, female, weighing 200-240 g) were control, sham-operated, MCAO (15 min occlusion + 24 hrs.reperfusion) and curcumin-treated pre-stroke group (received curcumin 300 mg/kg body weight/day, I/P, for30 days followed by MCAO). With the completion of the experimental protocol, sensorimotor deficits were examined by behavioral tests, including neurological deficit score, foot fault test, forelimb placing test, corner turn test, and wire hanging test. Results:Compared to MCAO rats, curcumin-treated MCAO rats showedbetter neurological functioning (p<0.05) as exhibited by substantial reductions in neurological score.Compared with stroke group,curcumin treated group showed betterfunctional outcomesasdisplayedby improvedscores in foot faultindex,andforelimb placing test (p<0.01), fewer left turns (p<0.01)in corner turn test, and prolongedgrip latency in wire hanging test(p<0.01).Conclusion:The present study showed that designed curcumin treatment effectively manages MCAO-induced sensorimotor dysfunction by preventing selective neuronal loss after the ischemic attack, attributed to its antioxidant, anti-apoptotic, and anti-inflammatory potentials.

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