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

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.