Abstract
Objective: Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease (AD). The present study was designed to investigate the neuroprotective effects of citrullus lanatus on bilateral common carotid artery occlusion (BCCAO) induced cognitive impairment and oxidative stress in Wistar albino rats.
 Methods: Cognitive impairment and oxidative stress were induced by BCCAO for 30 min, followed by 7 d reperfusion of male wistar rats. Morris water maze and rectangular maze performance tests and locomotor activity were used to assess memory performance tasks. To study the activity, rats weighing 250-300g were pre-treated with successive extracts of n-hexane fraction (HF), ethyl acetate fraction (EAF), ethanol fraction (EF) and aqueous fraction (AF) of 400 mg/kg, 200 mg/kg, p. o of each for 10 d and the treatment was continued for another 7 d after cerebral ischemia. Various biochemical parameters like lipid peroxidation, Catalase, DPPH and AchE were also estimated in the brain after the treatment.
 Results: There was significantly increased oxidative stress and cholinesterase activity with cognitive decline in the hippocampus in rats of BCCAO group as compared to sham-operated (p<0.05). The animals treated with Donepezil, HF and EF prevented the biochemical changes significantly (p<0.001) and there was significant (p<0.001) improvement in cognitive parameters compared to BCCAO treated rats.
 Conclusion: Thus present study indicates the neuroprotective effect of citrulus lanatus seed extract (HF and EF) against BCCAO induced cognitive impairment and associative oxidative damage.
Highlights
Alzheimer’s disease (AD) is a one of neurodegenerative disorder, it is associated with brain infarction
Citrullus lanatus (CL) various extract (HF, ethyl acetate fraction (EAF), ethanol fraction (EF), and aqueous fraction (AF) of 400 and 200 mg/kg, PO) treatments after cerebral ischemia significantly decreased the initial acquisition latency (IAL) to reach the platform in the pretrained rats as compared to bilateral common carotid artery occlusion (BCCAO) treated rats on day 12
The results suggest that BCCAO caused significant cognitive impairment
Summary
Alzheimer’s disease (AD) is a one of neurodegenerative disorder, it is associated with brain infarction. The global cerebral hypoperfusion with bilateral common carotid artery occlusion (BCCAO) induced cognitive impairment is a well-known model, which may induce BBB disruption, neuronal injury in the cortex and hippocampus, cause infarctions in the striatum of unstable sizes and elevated inflammatory responses since cognitive impairment is central in dementia [3]. This causes the death of neurons and related behavioral deficits including sensorimotor abnormality, spatial orientation disorder, and learning-memory impairments
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