急性奇昆古尼亚感染通过直接扰乱内皮细胞中的还氧化信号来诱导血管功能障碍
José Teles de Oliveira-Neto1, Juliano de P Souza2, Daniel Rodrigues1
1Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirão Preto 14040-900, Brazil.
Cells
|November 8, 2024
概括
奇孔古尼亚病毒感染通过改变氧化还原信号通路,特别是涉及活性氧物种 (ROS) 和氧化 (NO) 生产,从而导致心血管并发症,从而损害了血管功能.
科学领域:
- 心血管研究研究心血管研究
- 传染性疾病 传染性疾病
- 血管生物学 血管生物学
背景情况:
- 奇孔古尼亚病毒 (CHIKV) 感染导致发烧性疾病,关节疼痛和心血管并发症.
- 奇克病毒感染与活性氧物种 (ROS) 和细胞因子释放有关,可能会破坏血管平衡.
- 人们对CHIKV影响血管功能的确切机制尚不完全了解.
研究的目的:
- 调查CHIKV诱导动脉功能障碍的假设,通过直接影响血管细胞中与氧化还原相关的机制.
- 阐明诱导性氧化合成酶 (iNOS) 在CHIKV诱导的血管功能障碍中的作用.
- 检查CHIKV感染对血管ROS产生和信号通路的影响.
主要方法:
- 在体内研究中使用感染CHIKV或模拟载体的野生类型和iNOS敲击小鼠.
- 血管功能通过线筋图,血压测量和细胞因子,ROS和氧化的生物化学测试来评估.
- 在体外研究涉及CHIKV感染的内皮细胞,以分析蛋白质表达.
主要成果:
- 奇克病毒感染引发了显著的血管功能障碍,降低了缩血压,改变了细胞因子配置 (增加了IL-6和IFN-γ).
- 观察到明显的对烯的低反应性,这被INOS抑制或删除和内皮切除所阻止.
- CHIKV感染增加了血管超氧化和亚酸盐的产生,减少了过氧化,并提高了TBARS水平,表明氧化应激.
结论:
- 奇克病毒感染直接影响血管细胞,通过氧化还原相关机制的改变导致动脉功能障碍.
- 这项研究强调了ROS/NF-kB/iNOS/NO信号通路在CHIKV相关心血管并发症中的关键作用.
- 这些发现表明,针对这些途径可能提供治疗策略,用于管理心血管事件在奇孔古尼亚患者.
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