Now we just need our researchers to test this in humans for stroke, but your doctors and stroke hospital will do nothing. They prefer to be incompetent both in NOT KNOWING AND NOT DOING.
Neuroprotective effect of edible bird’s nest in chronic cerebral hypoperfusion induced neurodegeneration in rats
1Department of Basic Medical Sciences, International Islamic University Malaysia, Kuantan 25200, Malaysia.
2Department of Physiology, University Kebangsaan, Kuala Lumpour 5600, Malaysia.
3Department of pathology and Laboratory Medicine, International Islamic University Malaysia, Kuantan 25200, Malaysia.
4Department of Pharmaceutical Technology, International Islamic University Malaysia, Kuantan 25200, Malaysia.
5Clinical Pharmacology department, Menoufia University, Shebin Elkom 32511, Egypt.
Correspondence Address: Rehab A. Ismaeil, Department of Basic Medical Sciences, International Islamic University Malaysia, Kuantan-25200, Malaysia. E-mail: rehabpharma81@gmail.com
© The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
Abstract
Aim: Alzheimer’s disease (AD) is marked by insufficient blood supply to the brain, leading to progressive loss of memory and cognitive skills. The continuous reduction of cerebral blood flow resulting from chronic cerebral hypoperfusion leads to the overproduction of reactive oxygen species that triggers inflammation, causing cognitive decline. Till now, there is no cure for AD and the only option is symptomatic treatment. The current study evaluates the effect of edible bird’s nest (EBN) on hippocampal neurons, specifically in the CA1 hippocampal region, by using a rat model of chronic cerebral hypoperfusion-induced neuroinflammation.
Methods: Chronic cerebral hypoperfusion (CCH) was induced by permanent bilateral common carotid artery occlusion (2VO) in rats to trigger the neuroinflammatory process. Rats were divided into 4 groups: sham, 2VO, and two 2VO groups treated with two different doses (60 mg/kg, 120 mg/kg) of EBN, which was administered daily by oral gavage. After 8 consecutive weeks, rats were euthanized and the hippocampi were examined histopathologically by counting viable neuronal cells and the levels of F2- Isoprostane in hippocampal tissue was measured by ELISA.
Results: A significant decrease in neuronal cell death and a significant decline in F2-Isoprostane levels were observed in rats treated with EBN.
Conclusion: This is the first study to associate the neuroprotective effect of EBN in the prevention of dementia related to AD. EBN could be used as a complementary treatment to delay or treat dementia in AD patients.
Keywords
Alzheimer’s disease, chronic cerebral hypoperfusion, edible bird’s nest, F2-Isoprostanes
Introduction
The most prevalent neurodegenerative disorder that has dramatically increased over the last 60 years is Alzheimer’s disease (AD). AD is a chronic disorder that starts years before the detection of any clinical cognitive decline, with memory loss and a decline in cerebral blood supply[1-3]. Chronic cerebral hypoperfusion (CCH), along with various types of vascular insufficiency may initiate a cascade of events such as oxidative stress and inflammatory reactions that trigger vascular dementia[3-6]. As an established animal model for imitating the reduction in cerebral blood flow in human aging, permanent bilateral occlusion of common carotid arteries in rats (2-Vessel Occlusion, 2VO) has been introduced[7,8]. A continuous decrease in regional cerebral blood flow (CBF) in different areas in the rat brain including the cerebral cortex and hippocampus causes neuronal dysfunction and impairs spatial learning, leading to memory deficits and dementia[3,7,9]. Previous studies of neuropathological changes caused by CCH focused on the hippocampus due to its essential role in learning and memory[8,10-12]. Furthermore, the hippocampal CA1 area is the most vulnerable in CCH[11,13,14]. In order to diagnose and treat the pathophysiological changes of CCH in an animal model, the detection of essential biomarkers would have a critical role. F2-Isoprostanes (F2-IsoPs) are prostaglandin-like molecules that are formed from the peroxidation of arachidonic acid. IsoPs are considered an accurate predictor of lipid peroxidation due to their biological stability[13-16].
Recent alternative medicines have underscored the neuroprotective and anti-inflammatory ability of edible bird’s nest (EBN). EBN is one of the most valuable animal products eaten by humans, either for its therapeutic properties or as a delicacy in South East Asia[17,18]. It is formed naturally from salivary secretions of glutinous glycoprotein through the sublingual glands of swiftlets birds during their nesting and breeding season. The nest is built high on walls and the roofs of caves in the shape of a bowl over a period of 35 days. The solidified secretions enable the nest to carry the swiftlets and their eggs to remain attached to the wall during breeding season[17-19]. Researchers have investigated the therapeutic effects of EBN such as its anti-oxidative effect, anti-inflammatory effect, alleviation of osteoarthritis[20-22], increased proliferation of the uterus, the enhancement of cell proliferation in corneal wound healing[23,24] and its antiviral effect[25,26]. Moreover, it has the ability to reduce the risk of hypercoagulation caused by cardiovascular diseases associated with a high-fat diet[27]. Hou et al.[28] (2017) underscored the neuroprotective effect of EBN with elevated antioxidant activity in an ovariectomized rat model. EBN is also beneficial in reducing severity of neurodegenerative disorders due to its antioxidative effects on valuable bioactive components such as lactoferrin and ovotransferrin-like compounds[29]. Furthermore, sialic acid in EBN can enhance memory and improve cognitive function[30,31]. Additionally, EBN has epidermal growth factor-like activity, and is a rich source of proteins, carbohydrates, amino acids and minerals[18,32-34]. With such previous encouraging results, the current study investigated the neuroprotective and anti-inflammatory effects of EBN using a chronic cerebral hypoperfusion model. The occlusion of common carotid arteries triggers the formation of oxidative stress, causing inflammation in the brain hippocampus that then leads to neuronal death[6,11-14,35].
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