Water Extractable Phytochemicals from Peppers (Capsicum spp.) Inhibit Acetylcholinesterase and Butyrylcholinesterase Activities and Prooxidants Induced Lipid Peroxidation in Rat Brain In Vitro
Background. This study sought to investigate antioxidant capacity of aqueous extracts of two pepper varieties (Capsicum annuum var. accuminatum (SM) and Capsicum chinense (RO)) and their inhibitory effect on acetylcholinesterase and butyrylcholinesterase activities. Methods. The antioxidant capacity of the peppers was evaluated by the 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS) radical scavenging ability and ferric reducing antioxidant property. The inhibition of prooxidant induced lipid peroxidation and cholinesterase activities in rat brain homogenates was also evaluated. Results. There was no significant difference () in the total phenol contents of the unripe and ripe Capsicum spp. extracts. Ripe and unripe SM samples had significantly higher () ABTS scavenging ability than RO samples, while the ripe fruits had significantly higher () ferric reducing properties in the varieties. Furthermore, the extracts inhibited Fe2+ and quinolinic acid induced lipid peroxidation in rats brain homogenates in a dose-dependent manner. Ripe and unripe samples from SM had significantly higher AChE inhibitory abilities than RO samples, while there was no significant difference in the BuChE inhibitory abilities of the pepper samples. Conclusion. The antioxidant and anticholinesterase properties of Capsicum spp. may be a possible dietary means by which oxidative stress and symptomatic cognitive decline associated with neurodegenerative conditions could be alleviated. 1. Introduction Alzheimer’s disease (AD) is characterized by progressive cognitive, functional, and behavioral impairment, which evolves into a dramatic loss of most cortical and subcortical functions and, ultimately, death [1]. Demographic changes and the rise in life expectancy have resulted in the growth recorded in the number of individuals affected by AD. It is forecast that the worldwide number of elderly people suffering from dementia will rise to 63 million in 2030 and to 114 million in 2050 [2]. The socioeconomic impact associated with the global AD burden that cannot be estimated raises the need to find preventive and palliative means of treatment for sufferers. Deficiency of the neurotransmitter acetylcholine at the synaptic cleft coupled with cholinergic decline in the hippocampal and cortical regions of the brain is associated with cognitive decline observed in AD [3], a situation which is further aggravated by deposition of amyloid proteins observed in senile plaques in the extracellular matrix of the brain [4]. There is evidence that cholinesterase inhibitors (ChEIs) may slow
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