创伤性脑损伤
外渗
神经保护
促炎细胞因子
血脑屏障
医学
细胞外基质
下调和上调
药理学
血管通透性
肿瘤坏死因子α
埃文斯蓝
炎症
神经科学
免疫学
细胞生物学
病理
化学
内科学
中枢神经系统
生物
基因
生物化学
精神科
作者
Miranda D. Diaz,Rebecca M Kandell,Joseph C. Wu,Alexander Chen,Karen L. Christman,Ester J. Kwon
标识
DOI:10.1002/adhm.202300782
摘要
Abstract Traumatic brain injury (TBI) affects millions of people each year and, in many cases, results in long‐term disabilities. Once a TBI has occurred, there is a significant breakdown of the blood−brain barrier resulting in increased vascular permeability and progression of the injury. In this study, the use of an infusible extracellular matrix‐derived biomaterial (iECM) for its ability to reduce vascular permeability and modulate gene expression in the injured brain is investigated. First, the pharmacokinetics of iECM administration in a mouse model of TBI is characterized, and the robust accumulation of iECM at the site of injury is demonstrated. Next, it is shown that iECM administration after injury can reduce the extravasation of molecules into the brain, and in vitro, iECM increases trans‐endothelial electrical resistance across a monolayer of TNFα‐stimulated endothelial cells. In gene expression analysis of brain tissue, iECM induces changes that are indicative of downregulation of the proinflammatory response 1‐day post‐injury/treatment and neuroprotection at 5 days post‐injury/treatment. Therefore, iECM shows potential as a treatment for TBI.
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