Joó F, Tósaki A, Oláh Z, Koltai M
Laboratory of Molecular Neurobiology, Institute of Biophysics Biological Research Center, Szeged, Hungary.
Brain Res. 1989 Jun 19;490(1):141-3. doi: 10.1016/0006-8993(89)90439-3.
The effect of the protein kinase C enzyme inhibitor H-7 was examined on the brain edema formation evoked by bilateral occlusion of the common carotid arteries in Sprague-Dawley rats of CFY strain. Brain edema was assessed by measurement of water and electrolyte contents of the brain. The results showed that pretreatment with H-7 reduced the extent of brain edema formation in a dose-dependent manner. The fact that H-7 treatment prevented the accumulation of water and certain electrolytes in the brain indicates that the protein kinase C may be activated not only in the neuronal structures but also in the microvessels during ischemia, which can lead directly or via certain calcium-mediated mechanisms to the opening of tight junctions resulting in the development of brain edema.
在CFY品系的Sprague-Dawley大鼠中,研究了蛋白激酶C酶抑制剂H-7对双侧颈总动脉闭塞诱发的脑水肿形成的影响。通过测量脑内水和电解质含量来评估脑水肿。结果表明,用H-7预处理可剂量依赖性地减轻脑水肿形成的程度。H-7处理可防止脑内水和某些电解质的蓄积,这一事实表明,蛋白激酶C不仅可能在缺血期间在神经元结构中被激活,而且也可能在微血管中被激活,这可直接或通过某些钙介导的机制导致紧密连接开放,从而引发脑水肿。