Mechanism for HMGB-or HMGB1-derived peptide-induced increase in BBB permeability

一个代表性的损伤相关分子模式，高迁移率族蛋白1（HMGB1），从神经元核释放到细胞外空间通过细胞质缺血或创伤性脑损伤后。释放的HMGB1引起血管内皮细胞和周细胞的收缩反应，导致血脑屏障通透性增加。在HMGB1衍生肽中，有些具有多种活性。抗HMGB1单克隆抗体可抑制创伤性脑损伤引起的血脑屏障通透性和炎症反应。

A representative damage-associated molecular pattern, high mobility group box-1(HMGB1), was released from neuronal nuclei to extracellular space via cytosol after ischemia or traumatic brain injury. The released HMGB1 induced contractile response in vascular endothelial cells and pericytes leading to the increased permeability of BBB. Among HMGB1-derived peptides, some had plural activities. Anti-HMGB1 monoclonal antibody inhibited the BBB permeability and inflammatory responses induced by traumatic brain injury.