Krill Oil Attenuates Cognitive Impairment by the Regulation of Oxidative Stress and Neuronal Apoptosis in an Amyloid β-Induced Alzheimer’s Disease Mouse Model
Autor: | Eun Ju Cho, Ji Myung Choi, Mei Tong He, Dongjun Lee, Ji Hyun Kim, Hui Wen Meng |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
cognition
Pharmaceutical Science Morris water navigation task Apoptosis medicine.disease_cause Analytical Chemistry memory chemistry.chemical_compound Mice 0302 clinical medicine Drug Discovery oxidative stress chemistry.chemical_classification Neurons 0303 health sciences biology Behavior Animal krill oil Malondialdehyde Chemistry (miscellaneous) Fatty Acids Unsaturated Molecular Medicine Alzheimer’s disease medicine.medical_specialty Amyloid beta Oxidative phosphorylation Krill oil Article Nitric oxide lcsh:QD241-441 03 medical and health sciences lcsh:Organic chemistry Alzheimer Disease Internal medicine medicine Animals Cognitive Dysfunction Physical and Theoretical Chemistry Maze Learning 030304 developmental biology Reactive oxygen species Amyloid beta-Peptides business.industry Organic Chemistry amyloid beta Disease Models Animal Endocrinology chemistry biology.protein business Reactive Oxygen Species 030217 neurology & neurosurgery Oxidative stress Biomarkers Euphausiacea |
Zdroj: | Molecules Volume 25 Issue 17 Molecules, Vol 25, Iss 3942, p 3942 (2020) |
ISSN: | 1420-3049 |
DOI: | 10.3390/molecules25173942 |
Popis: | In the present study, we investigated the cognitive improvement effects and its mechanisms of krill oil (KO) in A&beta 25&ndash 35-induced Alzheimer&rsquo s disease (AD) mouse model. The A&beta 35-injected AD mouse showed memory and cognitive impairment in the behavior tests. However, the administration of KO improved novel object recognition ability and passive avoidance ability compared with A&beta 35-injected control mice in behavior tests. In addition, KO-administered mice showed shorter latency to find the hidden platform in a Morris water maze test, indicating that KO improved learning and memory abilities. To evaluate the cognitive improvement mechanisms of KO, we measured the oxidative stress-related biomarkers and apoptosis-related protein expressions in the brain. The administration of KO inhibited oxidative stress-related biomarkers such as reactive oxygen species, malondialdehyde, and nitric oxide compared with AD control mice induced by A&beta 35. In addition, KO-administered mice showed down-regulation of Bax/Bcl-2 ratio in the brain. Therefore, this study indicated that KO-administered mice improved cognitive function against A&beta 35 by attenuations of neuronal oxidative stress and neuronal apoptosis. It suggests that KO might be a potential agent for prevention and treatment of AD. |
Databáze: | OpenAIRE |
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