高表达Syndecan-1外泌体修复LPS介导的血管内皮细胞屏障功能损伤的研究

细菌内毒素可损害血管内皮细胞屏障功能，引起血管通透性增加，进而造成休克、急性肺损伤，但是其机理并不十分清楚。本研究在大鼠LPS肺损伤模型以及体外血管内皮细胞培养的基础上，观察LPS诱导血管内皮细胞Syndecan-1损伤情况，同时分析Syndecan-1与血管通透性、细胞内骨架蛋白、细胞连接蛋白等变化的关系；给予高表达Syndecan-1的血管内皮细胞外泌体，以期修复血管内皮细胞表面Syndecan-1蛋白，改善血管内皮细胞屏障功能。研究将阐明Syndecan-1损伤可能是感染后血管内皮细胞屏障功能受损的机理之一；利用高表达Syndecan-1外泌体能修复血管内皮细胞屏障功能，并可能成为干预脓毒症后脏器损伤的潜在途径。

The mechanism of LPS-induced micro-vascular endothelial injury is unclear. In the project, LPS-induced human micro-vascular endothelial barrier impairment, expression changes of cell junctions and F-actin, and Syndecans-1 depression are detected on both models of endothelium culture in vitro and LPS-induced rat lung injury in vivo. The relationship of Syndecan-1 depression and LPS-induced endothelial barrier impairment are analyzed at same time. Using Syndecan-1 high-expressing exosomes could repair LPS-induced endothelial barrier injury both in vitro and in vivo. Taken together,Syndecan-1 damage may be one of causes in LPS-induced micro-vascular endothelial barrier injury, and application of Syndecan-1 by vehicle of exosomes may be a potential way to intervene organs injury in sepsis.