2010 Fiscal Year Final Research Report

Pathophysiological study of lower limb ischemia-reperfusion injury

Research Project

Project/Area Number	20790464
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Legal medicine
Research Institution	Fukushima Medical University
Principal Investigator	KATO Naho Fukushima Medical University, 医学部, 助教 (20457766)
Project Period (FY)	2008 – 2010
Keywords	虚血再還流障害 / 挫滅症候群 / IL-6ノックアウトマウス / iNOSノックアウトマウス / リアルタイムPCR
Research Abstract	The mouse bilateral hind limb tourniquet-reperfusion model can be considered as an experimental animal model of crush syndrome. By using this model, we investigated mRNA expression levels of various inflammatory cytokines in the kidney, a damaged organ distant from the ischemic hind limb. So, we found that the expression level of kidney IL-6 mRNA increased and that of iNOS mRNA decreased after reperfusion. In contrast, survival rates 24 h after ischemia-reperfusion were in the order of iNOS-deficient mice≧C57Black/6J wild-type mice>IL-6-deficient mice. These results indicated that IL-6 plays an ameliorative role and that iNOS play a deteriorative role. This model shows a high mortality rate in mice, but morphological changes in the kidney, such as nuclear concentration of tubular epithelial cells and infiltration of inflammatory cells, were minor.

(5 results)