P-BN004. Neuroprotective effect of edible bird's nest on chronic cerebral hypoperfusion induced neurodegeneration in rats

• Published in: Clinical neurophysiology Vol. 132; no. 8; pp. e121 - e122
• Main Authors: Ismaeil, Rehab, Binti Ahmad Affandi, Khairunisa, Kien Hui, Chua, Mohamed, Wael, Fadly, Mohd
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.08.2021
• ISSN: 1388-2457; 1872-8952
• DOI: 10.1016/j.clinph.2021.02.299

Introduction. Alzheimer’s disease is marked by insufficient blood supply to the brain, leads to progressive loss of memory and cognitive skills. Continuous reduction of cerebral blood flow as a result of chronic cerebral hypoperfusion leads to overproduction of reactive oxygen species that may cause cognitive decline. Until now there is no available curative treatment for Alzheimer’s disease (AD) and the only available option is symptomatic treatment. Recent alternative medicines have underscored the neuroprotective and antioxidant ability of the edible bird’s nest (EBN). The current study evaluates the effects of EBN on hippocampal neurons specifically in the CA1 hippocampal region by using chronic cerebral hypoperfusion- induced neurodegeneration in rat model. Methods. Chronic cerebral hypoperfusion was induced by permanent bilateral common carotid arteries occlusion (2VO) in rats that triggers the neuroinflammatory processes. The rats were divided into 4 groups: Sham group, 2VO group, and two 2VO groups treated with 2 different doses (60,120 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 the viable neuronal cells and the level of F2 Isoprostane in hipoocampal tissue was measured by ELISA. Results. A significant decrease in the neuronal cell death and significant decline in F2 Isoprostane level was shown in the group of rats treated with EBN. Conclusion. CCH, which was triggered by 2VO, causes reduction in viable neurons in the hippocampal CA1 region. This damage could be ameliorated by administration of EBN, which exhibits a neuroprotective effect via increasing the viable neuronal cell count and decline in oxidative stress level. Our results underscored the possible effects of EBN in delaying the progression of dementia in AD patients if used early in the disease. It is safe supplement that could be used prophylactically for a long time.