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

Author

Yan Li ; Wei-Kang Wu

Author_Institution

Dept. of Pathophysiology, Bengbu Med. Coll., Bengbu, China

Volume

2

fYear

2011

fDate

9-11 Dec. 2011

Firstpage

584

Lastpage

587

Abstract

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.

Keywords

biochemistry; cellular biophysics; enzymes; injuries; lung; molecular biophysics; patient treatment; Huayu Tongho treatment; Jute lung injury treatment; MLCK pathway; Rho/Rho kinase; acute lung injury; cellular mechanism; collateral theory; endothelial barrier; endothelial cell cytoskeleton; hirudin protective effect; mice; molecular mechanism; pathophysiological mechanism; toxic stasis; transendothelial aggregation; ALI; DuYuSunLuo; Hirudin; LPS; MLCK; Rho/ROCK; cell cytoskeleton; endothelial barrier; polymorphonuclear leukocyte (neutrophil, PMN);

fLanguage

English

Publisher

ieee

Conference_Titel

IT in Medicine and Education (ITME), 2011 International Symposium on

Conference_Location

Cuangzhou

Print_ISBN

978-1-61284-701-6

Type

conf

DOI

10.1109/ITiME.2011.6132179

Filename

6132179