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The protective effect of hirudin on acute lung injury with collaterals damaged by toxic stasis in mice and its mechanism

机译:水rud素对小鼠急性中毒淤滞所致肺损伤的保护作用及其机制

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Firstly, we attempted to apply collaterals theory to monitor the treatment of a Jute lung injury (ALI), and proposed “DuYuSunLuo” hypothesis (collaterals damaged by toxic stasis) and “Huayu Tongho” treatment (dissolving stasis and activating collaterals) accordingly Secondly, based on literatures study, ft was critically analyzed that hirudin protected ALI in mice model. Next, we found that the pathophysiological mechanism of hirudin in ALI experimental model may be in part related to the protection of endothelial barrier and thus attenuating PMNs'' transendothelial aggregation in lung. Finally, we showed that inhibition of Rho/Rho kinase and MLCK pathway and protection of endothelial cell cytoskeleton plays an important role in cellular and molecular mechanisms of hirudin application in ALI.
机译:首先,我们尝试运用抵押品理论来监测黄麻肺损伤(ALI)的治疗,并提出了“独玉孙罗”假说(因中毒淤滞而损坏的抵押品)和“华裕通和”疗法(化瘀和激活抵押品)的相应说法。根据文献研究,严格分析了水rud素可保护小鼠模型中的ALI。接下来,我们发现ALI实验模型中水rud素的病理生理机制可能部分与保护内皮屏障有关,从而减弱了肺中PMNs的跨内皮聚集。最后,我们表明抑制Rho / Rho激酶和MLCK途径以及保护内皮细胞的细胞骨架在水rud素在ALI中的细胞和分子机制中起着重要作用。

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