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卡维奥林-1/NF-κB信号通路参与了由Lactobacillus casei细胞壁提取物诱导的川崎病血管炎

Shamin Wu¹, Xipo Chen¹, Kaixuan Wang²

¹Department of Pediatrics, Jinhua Maternal and Child Health Care Hospital, Zhejiang, China.

Modern rheumatology

|July 8, 2025

概括

卡维奥林-1 (Cav-1) 在川崎病 (KD) 血管炎中起着关键作用. 在小鼠模型中抑制Cav-1减少了炎症和NF-κB通路激活,这表明KD的治疗点.

科学领域:

血管生物学血管生物学
免疫学免疫学免疫学
儿科疾病儿科疾病

背景情况:

川崎病 (KD) 是一种急性血管炎,具有复杂的发病因子.
洞穴-1 (Cav-1) 是洞穴的关键结构蛋白,与血管疾病的发病有关.
在急性KD中血清Cav-1水平升高表明了潜在的作用,但其具体参与仍然不清楚.

研究的目的:

调查Caveolin-1 (Cav-1) 在川崎病 (KD) 病原发生中的作用.
探索Cav-1影响KD血管炎的机制.

主要方法:

川崎病 (KD) 血管炎在小鼠中被诱导使用 Lactobacillus casei 细胞壁提取物 (LCWE).
使用AAV-Cav-1shRNA.使用Caveolin-1 (Cav-1) 表达被抑制.
评估了心血管病变,细胞因子水平 (qRT-PCR),内皮细胞粘附分子 (免疫组织化学),Cav-1表达和NF-κB激活 (西方斑点).

主要成果:

在小鼠中,LCWE诱导的KD血管炎显示增加了Cav-1,促炎细胞因子,MMP-9和内皮细胞粘附分子.
抑制Cav-1可以逆转这些炎症标志物和心血管病变.
在KD血管炎中NF-κB通路的激活在Cav-1抑制后被抑制.

结论:

卡维奥林-1 (Cav-1) 参与了川崎病 (KD) 血管炎的发病.
卡维-1通过NF-κB信号通路调节KD血管炎.

关键词:

卡维奥林 - 1 - 一个洞穴.在 NF-κBB 中.内皮细胞粘附分子分子内皮细胞粘附分子卡瓦萨基疾病是卡瓦萨基疾病.有关炎症的细胞因子.

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