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S100钙结合蛋白A8加剧血管内皮细胞中的深静脉血栓形成。

S100 calcium-binding protein A8 exacerbates deep vein thrombosis in vascular endothelial cells.

作者信息

Chi Junyu, Wang Qitao, Wang Zhen, Zeng Wenjie, Gao Yangyang, Li Xin, Wang Wanpeng, Wang Jiali, Qu Ming

机构信息

Vascular Gland Surgery, The First Affiliated Hospital of Hebei North University, Zhangjiakou, 075000, Hebei, China.

Xiangya Hospital Central South University, Changsha, 410008, Hunan, China.

出版信息

Sci Rep. 2025 Jan 4;15(1):831. doi: 10.1038/s41598-025-85322-6.

Abstract

Previous studies highlighting the pivotal function of the S100A8 protein have shown that inflammation and vascular endothelial harm play a major role in deep vein thrombosis (DVT) development, as evidenced by earlier studies highlighting the pivotal function of the S100 calcium-binding protein A8 (S100A8). Therefore, we aimed to establish a connection between S100A8 and DVT and investigate the role of S100A8 in DVT development. Blood specimens were taken from 23 patients with DVT and 31 controls. The fluctuation and association for S100A8 and interleukin-1 beta (IL-1β) in the specimens was assessed using enzyme-linked immunosorbent assay. We also used the human recombinant protein S100A8 to activate human umbilical vein endothelial cells and created a rat model to explore the possible relationship between them. Studies have shown that the infiltration of S100A8 sustains local inflammation and thrombus formation, which may exacerbate DVT by amplifying NLRP3/Caspase-1/IL-1β signals in the vascular endothelial cells.

摘要

先前强调S100A8蛋白关键功能的研究表明,炎症和血管内皮损伤在深静脉血栓形成(DVT)过程中起主要作用,早期研究强调S100钙结合蛋白A8(S100A8)的关键功能已证明了这一点。因此,我们旨在建立S100A8与DVT之间的联系,并研究S100A8在DVT发展中的作用。采集了23例DVT患者和31例对照者的血液标本。使用酶联免疫吸附测定法评估标本中S100A8和白细胞介素-1β(IL-1β)的波动及相关性。我们还使用重组人蛋白S100A8激活人脐静脉内皮细胞,并建立大鼠模型以探索它们之间可能的关系。研究表明,S100A8的浸润维持局部炎症和血栓形成,这可能通过放大血管内皮细胞中的NLRP3/Caspase-1/IL-1β信号而加剧DVT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5496/11700128/21e00abd917f/41598_2025_85322_Fig1_HTML.jpg

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