Interaction between inducible nitric oxide synthase and cyclooxygenase-2 after cerebral ischemia
Interaction between inducible nitric oxide synthase and cyclooxygenase-2 after cerebral ischemia
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DOI：
10.1073/pnas.95.18.10966
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发表时间：
1998-09-01
影响因子：
11.1
通讯作者：
Iadecola, C
中科院分区：
文献类型：
--
作者：
Nogawa, S;Forster, C;Iadecola, C
局灶性脑缺血与诱导型一氧化氮合酶(INOS)和环氧合酶-2(COX-2)的表达有关，这两种酶的反应产物参与了缺血性脑损伤的演变。我们测试了这样的假设：脑缺血后，iNOS产生的一氧化氮(NO)增强了COX-2的活性，从而增加了这种酶的毒性潜力。用大鼠或小鼠大脑中动脉闭塞的方法造成脑缺血。大鼠脑缺血24小时后，iNOS免疫反应阳性的中性粒细胞近端可见(
Focal cerebral ischemia is associated with expression of both inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), enzymes whose reaction products contribute to the evolution of ischemic brain injury. We tested the hypothesis that, after cerebral ischemia, nitric oxide (NO) produced by iNOS enhances COX-2 activity, thereby increasing the toxic potential of this enzyme. Cerebral ischemia was produced by middle cerebral artery occlusion in rats or mice. Twenty-four hours after ischemia in rats, iNOS-immunoreactive neutrophils were observed in close proximity (