Takagi Y, Horikawa F, Nozaki K, Sugino T, Hashimoto N, Yodoi J
Department of Neurosurgery, Faculty of Medicine, Institute for Virus Research, Kyoto University, Sakyo, Japan.
Neurosci Lett. 1998 Jul 17;251(1):25-8. doi: 10.1016/s0304-3940(98)00492-3.
We assayed redox regulatory protein, thioredoxin (TRX) and TRX mRNA in the rat brain after transient and permanent middle cerebral artery (MCA) occlusion. The immunoreactivity for TRX and TRX mRNA disappeared after MCA occlusion in the ischemic core regions. On the other hand, in the perifocal ischemic regions, TRX immunoreactivity and TRX mRNA was enhanced. In addition, in transient MCA occlusion, TRX induction was stronger in the hippocampus and more widespread in the contralateral cortex than in permanent occlusion. Moreover, the induced TRX was translocated into the cellular nucleus after ischemia and ischemia-reperfusion. These results suggest that TRX induction was accompanied with reactive oxygen intermediates (ROI) overproduction and may play an important role not only in scavenging ROI but also in signal transduction during ischemia.
我们检测了短暂性和永久性大脑中动脉（MCA）闭塞后大鼠脑内的氧化还原调节蛋白、硫氧还蛋白（TRX）及其mRNA。在缺血核心区域，MCA闭塞后TRX的免疫反应性和TRX mRNA消失。另一方面，在灶周缺血区域，TRX免疫反应性和TRX mRNA增强。此外，在短暂性MCA闭塞中，海马体中TRX的诱导更强，对侧皮质中的诱导比永久性闭塞更广泛。而且，诱导的TRX在缺血和缺血再灌注后转移到细胞核中。这些结果表明，TRX的诱导伴随着活性氧中间体（ROI）的过量产生，并且可能不仅在清除ROI中起重要作用，而且在缺血期间的信号转导中也起重要作用。
