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人类抗原R增加的卡韦林1通过调节氧化应激和炎症反应加剧Porphyromonas gingivali诱导的动脉样硬化

Fang Miao¹, Yangyang Lei², Yunfei Guo¹

¹Department of Prevention and Healthcare, Lanzhou Stomatology Hospital, Lanzhou, China.

|December 31, 2024

概括

Porphyromonas gingivalis 感染会增加卡韦林1 (Cav-1) 的表达,从而促进动脉样硬化. HuR稳定了Cav-1,加剧了炎症和斑块形成,突出了与口腔疾病有关的心血管风险的关键机制.

科学领域:

心血管生物学心血管生物学
口腔微生物学口腔微生物学
疾病的分子机制.

背景情况:

由 Porphyromonas gingivalis 引起的慢性牙周炎与动脉样硬化 (AS) 有关.
P. gingivalis 影响了caveolin 1 (Cav-1) 和人类抗原R (HuR) 的表达,但它们在AS进展中的作用尚不清楚.

研究的目的:

研究Cav-1在P. gingivalis介导的AS进展中的作用和分子机制.
在这种情况下,阐明Cav-1和HuR之间的关系.

主要方法:

在人静脉内皮细胞 (HUVEC) 的体外感染与P. gingivalis和Cav-1沉默.
在体内使用阿波利波蛋白E缺陷AS模型小鼠的研究.
试验包括细胞活力,炎症,氧化应激,亡,Cav-1/ICAM-1水平,斑块形成以及Cav-1和HuR之间的分子相互作用.

主要成果:

P. gingivalis以时间和剂量依赖的方式诱导了Cav-1表达,抑制了HUVEC的扩散.
在HUVEC中,Cav-1干扰减少了炎症,活性氧物种 (ROS),ICAM-1水平和亡.
HuR稳定了Cav-1 mRNA,而增加的HuR则逆转了Cav-1沉默效应.
在小鼠模型中,抑制Cav-1降低了AS进展标志物.

结论:

HuR激活的Cav-1通过调节炎症反应和氧化应激来促进AS.
针对HuR-Cav-1通路可能为牙周炎相关的AS提供治疗策略.

关键词:

动脉样硬化是一种动脉样硬化.卡维奥林1 卡维奥林1 炎症炎症是一种炎症.葡萄牙牙牙病 Porphyromonas gingivalis 这种虫害的

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