C-phycocyanin Mitigates Cognitive Impairment in Doxorubicin-Induced Chemobrain: Impact on Neuroinflammation, Oxidative Stress, and Brain Mitochondrial and Synaptic Alterations
| Autor: | Yumei Liu, Sanqiang Li, Chenying Wang, Dongmei Wang, Shunji Pan, Lewei Wang, Yuhang Zhao |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male Dendritic spine Dendritic Spines Hippocampus Oxidative phosphorylation Mitochondrion Pharmacology medicine.disease_cause Biochemistry Neuroprotection 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Chemotherapy-Related Cognitive Impairment Morris Water Maze Test polycyclic compounds medicine Animals Cognitive decline Neuroinflammation Inflammation business.industry Phycocyanin General Medicine Mitochondria Mice Inbred C57BL Oxidative Stress 030104 developmental biology Neuroprotective Agents Doxorubicin Synapses business 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Neurochemical research. 46(2) |
| ISSN: | 1573-6903 |
| Popis: | Chemotherapy-induced cognitive impairment (CICI) is a common detrimental effect of cancer treatment, occurring in up to 75% of cancer patients. The widely utilized chemotherapeutic agent doxorubicin (DOX) has been implicated in cognitive decline, mostly via cytokine-induced neuroinflammatory and oxidative and mitochondrial damage to brain tissues. C-phycocyanin (CP) has previously been shown to have potent anti-inflammatory, antioxidant, and mitochondrial protective properties. Therefore, this present study was aimed to investigate the neuroprotective effects of CP against DOX-elicited cognitive impairment and explore the underlying mechanisms. CP treatment (50 mg/kg) significantly improved behavioral deficits in DOX-treated mice. Furthermore, CP suppressed DOX-induced neuroinflammation and oxidative stress, mitigated mitochondrial abnormalities, rescued dendritic spine loss, and increased synaptic density in the hippocampus of DOX-treated mice. Our results suggested that CP improves established DOX-induced cognitive deficits, which could be explained at least partly by inhibition of neuroinflammatory and oxidant stress and attenuation of mitochondrial and synaptic dysfunction. |
| Databáze: | OpenAIRE |
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