肥胖是多发性硬化症的一个可修改的危险因素吗? 对神经炎症和氧化损伤的机制性洞察
Fani-Niki Varra1,2, Olga Pagonopoulou3, Michail Varras4
1Department of Pharmacy, School of Health Sciences, Frederick University, Nicosia 1036, Cyprus.
概括
肥胖通过促进慢性炎症和氧化应激加剧多发性硬化症 (MS). 用多功能化合物准这些途径可能为这两种疾病提供新的治疗策略.
科学领域:
- 神经免疫学 神经免疫学
- 代谢障碍 代谢障碍 代谢障碍
- 慢性炎症性疾病 慢性炎症性疾病
背景情况:
- 多发性硬化症 (MS) 是一种中枢神经系统自身免疫性疾病,受遗传学,环境和生活方式的影响.
- 肥胖是一种与MS病理生理学相关的慢性炎症状况.
- 了解肥胖和MS之间的分子联系至关重要.
研究的目的:
- 分析肥胖和MS病理生理学之间的分子关系.
- 在分子水平上阐明肥胖和MS之间的复杂联系.
主要方法:
- 对PubMed和谷歌学者数据库的文献评论.
- 对连接肥胖和MS的分子机制的分析.
主要成果:
- 肥胖会引发慢性炎症,氧化应激 (OS) 和血脑屏障的破坏.
- 脂肪组织分泌着与MS相关的炎症性细胞因子和脂肪因子.
- 共同的炎症途径将肥胖和MS的发病方式联系起来.
结论:
- 肥胖是通过共同的潜在机制来改变多发性硬化症的风险因素.
- 多功能抗氧化和抗炎化合物显示出减缓多发性硬化症进展的潜力.
- 针对共享途径可能为肥胖和MS提供治疗选择.
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