Neuroprotective effect of edible bird’s nest in chronic cerebral hypoperfusion induced neurodegeneration in rats

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 tri...

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Bibliographic Details
Main Authors: Ismaeil, Rehab A., Chua, Kien Hui, Ahmad Affandi, Khairunisa, Alallam, Batoul, Mohamed, Wael Mohamed Yousef, Mohd Noor, Mohd Fadly
Format: Article
Language:en
Published: OAE Publishing Inc. 2021
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Online Access:http://irep.iium.edu.my/88923/14/88923_Ismaeil-2021-Neuroprotective-effect-of-edible-bi.pdf
http://irep.iium.edu.my/88923/
https://nnjournal.net/article/view/3916
http://dx.doi.org/10.20517/2347-8659.2020.63.
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Summary: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.