Báo cáo y học: "CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin/ICAM-1 deficient mice"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin/ICAM-1 deficient mice. | Journal of Inflammation BioMed Central Research CXC-chemokine regulation and neutrophil trafficking in hepatic ischemia-reperfusion injury in P-selectin ICAM-1 deficient mice Keith M Monson Shadi Dowlatshahi and Elahé T Crockett Open Access Address Department of Physiology College of Human Medicine Michigan State University East Lansing Michigan USA Email Keith M Monson - Shadi Dowlatshahi - dowlatsh@ Elahé T Crockett - ecrocket@ Corresponding author Published 24 May 2007 Received 30 January 2007 Journal of Inflammation 2007 4 11 doi 1476-9255-4-11 Accepted 24 May 2007 This article is available from http content 4 1 1 1 2007 Monson et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Neutrophil adhesion and migration are critical in hepatic ischemia and reperfusion injury I R . P-selectin and the intercellular adhesion molecule ICAM -1 can mediate neutrophil-endothelial cell interactions neutrophil migration and the interactions of neutrophils with hepatocytes in the liver. Despite very strong preclinical data recent clinical trials failed to show a protective effect of anti-adhesion therapy in reperfusion injury indicating that the length of injury might be a critical factor in neutrophil infiltration. Therefore the aim of this study was to assess the role of P-selectin and ICAM-1 in neutrophil infiltration and liver injury during early and late phases of liver I R. Methods Adult male wild-type and P-selectin ICAM-1-deficient P I null mice underwent 90 minutes of partial liver ischemia followed by various periods of reperfusion 6 15 h and a survival study . Liver injury was assessed by plasma level of alanine aminotransferase .

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