从分子生物学角度探究ALI/ARDS的发病机制

Exploration of ALI/ARDS Pathogenesis:From the Perspective of Molecular Biology

急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)的发病与如下机制相关,水通道蛋白在肺内液体的吸收及转运方面具有重要的作用,AQP-1、AQP-5可能参与了ALI液体的异常转运。在细胞因子中,肿瘤坏死因子α被认为是重要的ALI时早期释放的细胞因子,白细胞介素6和白细胞介素10具有抗炎作用,白细胞介素8水平升高与ALI的发病率和病死率密切相关,可溶型fractalkine分子被认为在ALI的炎性反应中发挥着重要作用。肺脏中性粒细胞参与了ALI的发生、发展,中性粒细胞弹性蛋白酶通过破坏或分解肺表面活性物质增加肺泡表面张力,促进血液的渗漏,导致ALI/ARDS。

The pathogenesis of acute lung injury（ALI）and acute respiratory distress syndrome（ARDS）is associated with water channel protein that has a critical role in intrapulmonary fluid absorption and transportation,in addition to the involvement of AQP-1 and AQP-5 in the abnormal transportation of fluid in AIL.Tumor necrosis factor α,a cytokine,is thought to be released in early ALI;interleukin-6 and 10 have anti-inflammatory activities;the increased interleukin-8 is closely associated with the incidence and mortality of ALI;soluble fractalkine plays a critical role in the inflammatory response of ALI.Pulmonary neutrophils are involved in the occurrence and development of ALI,which destruct or degrade the surfactants with elastase,resulting in the increase in alveolar surface tension,the occurrence of blood leakage and the progress of ALI/ARDS.