Ameliorative effects of astaxanthin on brain tissues of alzheimer’s disease-like model: cross talk between neuronal-specific microRNA-124 and related pathways
| Autor: | H.M. Osman, Shimaa A. Mahmoud, Samar S. Elblehi, Mohamed Osman, Hala A. Hafez, Maher A. Kamel |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
biology Monoamine oxidase Clinical Biochemistry Morris water navigation task Cell Biology General Medicine Pharmacology Acetylcholinesterase Neuroprotection Symptomatic relief 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine chemistry 030220 oncology & carcinogenesis medicine Amyloid precursor protein biology.protein Serotonin Molecular Biology Acetylcholine medicine.drug |
| Zdroj: | Molecular and Cellular Biochemistry. 476:2233-2249 |
| ISSN: | 1573-4919 0300-8177 |
| Popis: | Alzheimer’s disease (AD) is a chronic, progressive, multifactorial, and the most common neurodegenerative disease which causes dementia and mental deterioration in the elderly. The available treatments for AD are not disease-modifying drugs and only provide symptomatic relief. Astaxanthin (ATX), a second-generation antioxidant, is a dark red carotenoid and exhibits the highest antioxidant capacity, anti-inflammatory, neuroprotective, and antiapoptotic effects. In this study, we investigated the therapeutic effect of different doses of ATX on the cerebral cortex and hippocampus of AD-like rats. The AD-like model was induced in rats using hydrated aluminum chloride (AlCl3.6H2O) solution that was given orally at a dose of 75 mg/kg daily for 6 weeks. Morris water maze (MWM) behavioral test was performed to confirm the cognitive dysfunction then AD-like rats were orally treated with different doses of ATX (5, 10, and 15 mg/kg) dissolved in dimethyl sulfoxide (DMSO) for six weeks. The results indicated that ATX significantly and dose-dependently improved the performance of AD-like rats treated with ATX during MWM and suppress the accumulation of amyloid β1-42 and malondialdehyde. Also, significantly inhibit acetylcholinesterase and monoamine oxidase activities and the expression of β-site amyloid precursor protein cleaving enzyme 1 (BACE 1). ATX also significantly elevated the content of acetylcholine, serotonin, and nuclear factor erythroid-2-related factor 2 (Nrf2) and miRNA-124 expression. The effect of ATX treatment was confirmed by histopathological observations using H&E stain and morphometric tissue analysis. From this study, we concluded that ATX may be a promising therapeutic agent for AD through targeting different pathogenic pathways. |
| Databáze: | OpenAIRE |
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