흰쥐의 왼넙다리곧은근에서 반복적인 허혈양상화가 Cu,ZnSOD와 MnSOD의 발현에 미치는 영향
Effects of Repetitive Ischemic Preconditioning on the Expression of Cu,ZnSOD and MnSOD in Rectus Femoris Muscles of Rats
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세포에서 항산화계를 활성화시켜 산화적 손상을 감소시키는 것으로 알려진 허혈양상화가 반복되면서 흰 쥐 왼넙다리곧은근에서 나타나는 Cu,ZnSOD와 MnSOD의 변화양상을 알아보기 위하여 본실험을 실시하였다. 9주령과 35주령의 Sprague-Dawley계 수컷 흰쥐를 사용하여 왼온엉덩동맥에 5분의 허혈과 5분의 재관류를 3회, 6회, 10회 반복하여 허혈양상화시켰다. 허혈양상화 처치 직후, 3시간, 6시간, 24시간과 72시간 동안 재관류 후 왼넙 다리곧은근을 적출하여, 파라핀 절편을 만들고 Cu,ZnSOD와 MnSOD에 대한 면역조직화학염색을 시행하여 다음과 같은 결과를 얻었다. Cu,ZnSOD의 면역반응은 정상대조군의 9주령에서 중등도 이었고, 35주령에서는 매우 강하게 나타났으며, 3회와 6회 허혈양상화시 9주령과 35주령에서 재관류 3시간과 24시간 경과시 감소하였고, 10회 허혈양상화시 9주령은 감 소하였으나 35주령은 증가하였다. MnSOD의 면역반응은 정상대조군의 9주령과 35주령에서 중등도이었고 3회와 6회 허혈양상화시 재관류 24시간 경과후 감소하였으며 10회 허혈양상화시 9주령은 증가하였으나 35주령은 감소 하였다. Cu,ZnSOD의 변동폭은 3회 허혈양상화시킨 9주령과 10회 처치한 35주령에서 가장 컸고, MnSOD의 변동 폭은 6회 허혈양상화시킨 9주령군에서 가장 컸다. 이상의 실험결과에서 허혈양상화의 허혈손상 감소효과를 모두 설명할 수 없으나 10회 허혈양상화시킨 흰쥐의 경 우 9주령에서는 Cu,ZnSOD의 발현이, 35주령에서 MnSOD의 발현이 감소하여 손상이 일어나는 것으로 생각되었다.
Abstract
The present study was performed to investigate the dynamics of Cu,ZnSOD and MnSOD expression following courses of reperfusion after repetitive ischemic preconditioning on the left rectus femoris muscle of Spraque-Dawley rats. Nine or thirty five weeks-old rats were subjected to three, six and ten cycles of ischemic preconditioning that was 5 min ischemia and 5 min reperfusion at the left common iliac artery. Left rectus femoris muscle was isolated 0, 3, 6, 24 and 72 hours of reperfusion after ischemic preconditioning and assayed by immunohistochemical staining with anti- Cu,ZnSOD and anti-MnSOD antibodies. The results were as follows; The immunoreactivities of Cu,ZnSOD and MnSOD were increased in the repectitive three and six cycles of ischemic preconditioning. However, after the repetitive ten cycles of ischemic preconditioning, the Cu,ZnSOD immunoreactivities were decreased in the nine weeks-old rats while MnSOD immunoreactivities were decreased in thirty five weeks-old rats. These findings suggest that severe damayes result from decrease of Cu,ZnSOD in nine weeks-old rats and decrease of MnSOD in thirty five weeks-old rats after ten cycles of ischemic preconditioning.
참고문헌 (27)
- "Postischemic recovery of contractile function is impaired in SOD2(+", -) but not SOD1(+, pp.2002., 105[DOI]
- "Protective mechanismsduring ischemic tolerance in skeletal muscle.", 36, pp.371~379 (2004)
- "Limitations of ischemic tolerance in oxidative skeletal muscle: perfusion vs tissue protection.", 109, pp.62~67 (2003)
- "Overexpression of MnSOD protects againstmyocardial ischemia", reperfusion injury in transgenicmice., 1998., pp.30, 2281~2289
- "Preconditioning decreases ischemia", reperfusion-induced peroxynitrite formation., 2001., pp.285, 1217~1219
- "The effects of preconditioningon the oxidative stress in small-bowel autotransplantation.", 132, pp.877~884 (2002)
- "The cytosolic antioxidant copper", zinc-superoxide dismutase prevents the early release of mitochondrial cytochrome c in ischemic brain after transient focal cerebral ischemia in mice., 2000., pp.20, 2817~2824
- "Inflammatory and redoxresponses to ischaemia", reperfusion in human skeletal muscle, 2004., pp.107, 497~503
- "Increased ischemia-reperfusion blood flow impairs the skeletal muscle contractile function.", 99, pp.1~6 (2001)
- "Effect of nitric oxide on the contractile function of rat reperfused skeletal muscle", 106, pp.82~85 (2002)
- "patterns of injury in relation to adequacy of reperfusion.Exp Mol Pathol 44", pp.272~280 (1986)
- "Neonatal mouse cardiac myocytes exhibit cardioprotection induced by hypoxic and pharmacologic preconditioning and by transgenic overexpression of human Cu", Zn superoxide dismutase, 2000., pp.32, 1779~1786
- "Attenuation of focal cerebral ischemic injury in transgenicmice overexpressing CuZn superoxide dismutase.Proc Natl Acad Sci USA 88", ki(uchi h), pp.11158~11162 (1991), Epstein CJ
- "Protective effects of ischemic preconditioning on donor lung in canine lung transplantation.", 113, pp.1356~1359 (1998)
- "Endothelialprotection from reperfusion injury by ischemic preconditioningand diazoxide involves a SOD-like anti-O2-mechanism.", 55, pp.537~550 (2004)
- "Copper-zinc superoxide dismutase affects Akt activation after transient focal cerebral ischemia in mice", 34, pp.1513~1518 (2003)
- "Change in SOD Immunoreactivities of proximal anddistal muscles at occlusive of the hind limb after 2 hoursischemia and timely reperfusion.", 10, pp.93~111 (1997)
- "Ischemicpreconditioning reduces O2- generation and prevents respiratoryimpairment in the mitochondria of post-ischemicreperfused heart of rat.", 60, pp.2207~2219 (1997)
- "Ischemic tolerance in skeletal muscle role of nitric oxide.", 275 (1998)
- "Brain ischemic preconditioning is abolished by antioxidant drugs but does not up-regulate superoxide dismutase and glutathion peroxidase.", 1027, pp.30~37 (2004)
- "Overexpression of copper", zinc superoxide dismutase intransgenic mice protects against neuronal cell death aftertransient focal ischemia by blocking activation of the Badcell death signaling pathway., 2003., pp.23, 1710~1718
- "Effects ofmultiple cyclic episodes with short ischemia and reperfusionon the distribution of NF-κB Bcl-2 and Bax inrectro femoris muscles of rats.", 18, pp.45~55 (2005)
- "Effect ofaging on intestinal ischemia and reperfusion injury.", 107, pp.37~50 (1999)
- "Overexpression of human copper, zincsuperoxide dismutase (SOD1) prevents postischemic injury.", 95, pp.4556~4560 (1998)
- "A“second window of protection” occurs 24 h after ischemicpreconditioning in the rat heart.", 30, pp.1181~1189 (1998)
- "Induction of manganesesuperoxide dismutase in rat cardiac myocytes increasestolerance to hypoxia 24 hours after preconditioning. J ClinInvest 94", pp.2193~3199 (1994)
- "Modulationof liver oxidant-antioxidant system by ischemicpreconditioning during ischemia", reperfusion injury in rats., 2005., pp.11, 1825~1828
