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지구성 운동 유발 전 처치에 따른 심장보호 효과 (iNOS knock-out mice 활용)
김철현 ( Chul Hyun Kim ),엄현섭 ( Hyun Sub Um ),이영익 ( Young Ik Lee ),김윤만 ( Yoon Man Kim ),조인호 ( In Ho Cho ),김명기 ( Myung Ki Kim ),이규성 ( Kyu Sung Lee ),양대승 ( Dea Seung Yang ),오윤선 ( Yoon Sun Oh ),오유성 ( Yoo Sun 한국운동영양학회 2005 Physical Activity and Nutrition (Phys Act Nutr) Vol.9 No.1
The goal of this study was to explore the role of inducible NOS (iNOS) and the delayed protection of exercise preconditioning from the relative myocardial ischemia reperfusion injury. Mice were randomly placed in one of five testing groups: wild-type mice group (n = 15), high-intensity wild-type mice acute exercised group (n = 6). low-intensity wild-type mice acute exercised group (n = 5), L-NAME + wild-type mice acute exercised group (11 = 5), and homozygous (-/-) iNOS gene knock-out mice acute exercised group (n = 5). All acute exercised groups ran on the treadmill (0% grade) at 65 m,`min as a high-intensity exercise and at 27-30 m/min as a low-intensity exercise. The results showed that all acute exercise significantly reduced magnitude of a myocardial infarction in biphasic manner. In accordance with these data, NFKB and HSP-70 protein expression was increased at 24 after exercise-induced preconditioning (PC) in both low-intensity wild-type mice acute exercised group and homozygous (-/-) iNOS gene knock-out mice acute exercised group compared with wild-type mice group. In contrast, neither endothelial nitric oxide synthase (eNOS) nor inducible nitric oxide synthase (iNOS) expression changed at both wild-type mice group and low-intensity wild-type mice acute exercised group. In conclusion, The strong evidence of this study indicates that HSP-70 is particulary cytoprotectiye against protein-damaging stress such as I-R. Also, this study demonstrate that the late phase of exercise-induced PC is not associated with up-regulation of eNOS and iNOS but infarct-sparing effect and mild up-regulation of NFKB and HSP-70 at the late phase of exercise-induced PC in wild-type mice and iNOS gene knock-out mice. Thus, this study identifies a specific protein that mediates late PC in vitro.
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