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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:血红素对小鼠毒性瘀血损伤急性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,我们试图申请抵押理论来监测黄麻肺损伤(ALI)的治疗,并提出“DuyusunLuo”假设(毒性陷阱损坏的抵押品)和“华宇通孔”治疗(溶解僵局和激活抵押品),其次,基于文献研究,FT受到严格分析的是,在小鼠模型中受到血红素保护的Ali。接下来,我们发现血红素在ALI实验模型中的病理生理机制可以部分地与内皮屏障的保护有关,从而衰减PMNS的肺部颅骨胸腺聚集。最后,我们表明rhO / rhO激酶和MLCK途径的抑制和内皮细胞细胞骨架的保护在阿里河流应用中的细胞和分子机制中起着重要作用。

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