Abstract
Chronic stress exposure is now accepted as a problem that can produce deleterious effects on both brain structure and function. Numerous studies have proposed the potential of fruit peels as vital sources for acetylcholinesterase (AChE) inhibitors and antioxidants. Clausena lansium (Lour.) or wampee (WP) fruit peel is a rich source of antioxidants and flavonoids that could prove beneficial for human health. Currently, there has been no scientific evidence supporting the potency of WP peel extract to combat or reverse the memory impairment induced by chronic restraint stress (CRS). Therefore, we aimed to investigate the AChE-inhibiting and neuroprotective effects of WP peel extracts against CRS-mediated oxidative stress and cognitive dysfunction in rats. Initial assessment of the extract revealed antioxidant capacity and high concentrations of polyphenols. Further, Wistar rats were dosed orally with the WP peel extract (200, 400, and 600 mg/kg daily) and kept in a restrainer for 4 h a day for 28 consecutive days. The object recognition and Morris water maze tests were used to determine cognitive functions. After sacrifice, biomarkers of oxidative stress and AChE inhibitory activity in brain homogenates of rats were also investigated. CRS exposure produced oxidative stress and increased AChE activity, changes that led to learning and memory impairment in the cognition tests. Improved memory, reduced AChE activity, and a decreased oxidative stress status were seen in rats treated with WP peel extract. Overall, supplementation with WP peel extract may exert cognitive-enhancing effects through antioxidative neuroprotection and inhibition of AChE activity against CRS-induced oxidative stress.
Highlights
Exposure to chronic stress is a risk factor for the development of memory deficits (Azman et al, 2018)
This study explored the ability of WP peel extract to combat memory impairment induced by chronic restraint stress (CRS) through the inhibition of AChE activity or reduction of oxidative stress in rat brains
Acetylthiocholine iodide (ATCI), bovine serum albumin (BSA), 5,50dithiobis (2-nitrobenzoic acid) (DTNB), 2,2-diphenyl-1-picrylhydrazyl (DPPH), the Folin–Ciocalteu reagent (FCR), thiobarbituric acid (TBA), 2,4-dinitrophenylhydrazine (DNPH), gallic acid, and vitamin C were purchased from Sigma-Aldrich
Summary
Exposure to chronic stress is a risk factor for the development of memory deficits (Azman et al, 2018). Chronic stress suppresses early long-term potentiation (LTP) (Pavlides et al, 2002), but it reduces synaptic plasticity in the hippocampus (Wang et al, 2019). Chronic stress exposure induces reactive oxygen species (ROS) overproduction and lowers brain antioxidant enzymes activities, alterations that have been associated with cognitive impairment (Wang et al, 2014). The neurotransmitter acetylcholine (ACh) plays an important role for the maintenance of accurate cognitive functions. In vitro and in vivo studies have shown that increased acetylcholinesterase (AChE) levels result in learning deficits and memory impairment (Croxson et al, 2011). Acetylcholinesterase inhibitors (AChEIs) have been the mainstays of symptomatic therapy for cognitive disorders (Ashford, 2015)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
