Astaxanthin Ameliorates Doxorubicin-Induced Cognitive Impairment (Chemobrain) in Experimental Rat Model: Impact on Oxidative, Inflammatory, and Apoptotic Machineries
| Autor: | Sara A. Wahdan, Amal Kamal Abdel-Aziz, Samar S. Azab, Sara Emad El-Agamy, Ahmed Esmat |
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| Rok vydání: | 2017 |
| Předmět: |
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0301 basic medicine Antioxidant medicine.medical_treatment Anti-Inflammatory Agents Neuroscience (miscellaneous) Apoptosis Motor Activity Xanthophylls Pharmacology Biology medicine.disease_cause Hippocampus Models Biological Neuroprotection Antioxidants 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Glial Fibrillary Acidic Protein polycyclic compounds medicine Animals Memory impairment Cognitive Dysfunction Doxorubicin Neuroinflammation Inflammation Behavior Animal Neurotoxicity medicine.disease Rats Disease Models Animal Oxidative Stress Neuroprotective Agents 030104 developmental biology Neurology Nerve Degeneration Immunology Acetylcholinesterase Biomarkers 030217 neurology & neurosurgery Oxidative stress medicine.drug |
| Zdroj: | Molecular Neurobiology. 55:5727-5740 |
| ISSN: | 1559-1182 0893-7648 |
| Popis: | Chemobrain refers to a common sequelae experienced by 15-80% of cancer patients exposed to chemotherapeutics. The antineoplastic agent doxorubicin (DOX) has been implicated in a strenuous neurotoxicity manifested as decline in cognitive functions, most probably via cytokine-induced oxidative and nitrosative damage to brain tissues. Astaxanthin (AST), a naturally occurring carotenoid, is reputable for its outstanding antioxidant, anti-inflammatory, and antiapoptotic activities. Therefore, the aim of the current study was to investigate the potential neuroprotective and memory-enhancing effects of AST against DOX-induced behavioral and neurobiological abnormalities. Briefly, AST treatment (25 mg/kg) significantly protected against DOX-induced memory impairment. Furthermore, AST restored hippocampal histopathological architecture, halted DOX-induced oxidative and inflammatory insults, mitigated the increase in acetylcholinesterase activity, and consistently downregulated the overactive apoptotic machineries. In conclusion, these findings suggest that AST offers neuroprotection against DOX-induced cognitive impairment which could be explained at least partly by its antioxidant, anti-inflammatory, and antiapoptotic effects. |
| Databáze: | OpenAIRE |
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