氧化应激参与多发性硬化症的分子病原和进展:一篇文献综述
Alfredo Sanabria-Castro1,2, Alberto Alape-Girón3, Marietta Flores-Díaz3
1Unidad de Investigación, Hospital San Juan de Dios, Caja Costarricense de Seguro Social, San José, 10103, Costa Rica.
Reviews in the neurosciences
|January 1, 2024
概括
氧化应激通过损害中枢神经系统细胞并促进炎症,显著导致多发性硬化症 (MS). 抗氧化剂疗法在多发性硬化症治疗中表现有前途,需要进一步的临床评估.
科学领域:
- 神经免疫学 神经免疫学
- 自身免疫性疾病的病理生理学
- 氧化应激机制 氧化应激机制
背景情况:
- 多发性硬化症 (MS) 是一种慢性中枢神经系统自身免疫性疾病.
- 关键的病理特征包括炎症,脱髓化和神经退行.
- 氧化应激是MS发展和进展的关键因素.
研究的目的:
- 为提供MS中氧化应激的综合性审查.
- 阐明MS中氧化剂参与的细胞和分子机制.
- 讨论抗氧化剂对MS的治疗潜力.
主要方法:
- 关于细胞和分子机制的文献综述.
- 在MS病理生理学中氧化应激的分析.
- 对神经细胞和炎症的有害影响的评估.
主要成果:
- 氧化物种通过线粒体功能障碍,信号通路中断和免疫激活驱动MS的启动和进展.
- 氧化应激会损害神经元,寡细胞和星球细胞.
- 氧化剂在MS中延续炎症,脱髓化和轴突损伤.
结论:
- 氧化应激是多发性硬化症病理生理学的关键因素.
- 用抗氧化剂准氧化应激是一种潜在的MS治疗策略.
- 需要进一步的临床试验来验证合成抗氧化剂在MS患者中的有效性.
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