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多形核嗜中性白细胞(PMNs)和成人呼吸窘迫综合征(ARDS)发病有关,组织学上表明ARDS起因于邻近受损的肺内皮大量的PMNs。被激活的PMNs介导内皮细胞(EC)损伤和死亡,在全身炎症反应综合征时可导致血管通透性增加和毛细管渗漏。热休克反应是机体的防御机制,通过合成细胞内人热休克蛋白-72(HSP-72),促进启动损伤组织修复。本文目的是检验这种假设,即通过体外热休克或亚砷酸钠盐(sodium arsenite)诱导人EC内HSP-72的
Polymorphonuclear neutrophils (PMNs) are involved in the pathogenesis of adult respiratory distress syndrome (ARDS), and histologically suggest that ARDS results from the presence of large numbers of PMNs adjacent to the damaged lung endothelium. Activated PMNs mediate endothelial cell (EC) damage and death, leading to increased vascular permeability and capillary leakage in the systemic inflammatory response syndrome. Heat shock response is the body’s defense mechanism, through the synthesis of intracellular human heat shock protein -72 (HSP-72), to promote the injury tissue repair. The purpose of this paper is to test the hypothesis that the induction of HSP-72 in human ECs by in vitro heat shock or sodium arsenite