Protective effect of fasudil, a Rho-kinase inhibitor, on chemokine expression, leukocyte recruitment, and hepatocellular apoptosis in septic liver injury.

摘要: Rho-kinase signaling regulates important features of inflammatory reactions. Herein, we investigated the effect and mechanisms action inhibitor fasudil in endotoxemic liver injury. C57/BL/6 mice were challenged with lipopolysaccharide (LPS) D-galactosamine, or without pretreatment fasudil. Six hours after endotoxin challenge, leukocyte-endothelium interactions hepatic microvasculature studied by use intravital fluorescence microscopy tumor necrosis factor {alpha} (TNF-{alpha}); CXC chemokines as well enzymes apoptosis determined. Administration reduced LPS-induced leukocyte adhesion postsinusoidal venules sequestration sinusoids. Moreover, found that abolished extravascular infiltration leukocytes production TNF-{alpha} mice. Liver hepatocellular markedly reduced, sinusoidal perfusion was improved significantly pretreated Our novel data document is a potent endotoxin-induced expression liver. Based on present findings, it suggested inhibition pathway may be useful target treatment septic (Less)