Sun G Y, Lin T A, Wixom P, Zoeller R T, Lin T N, He Y Y, Hsu C Y
Department of Biochemistry, University of Missouri, Columbia 65212.
Ann N Y Acad Sci. 1993 May 28;679:382-7. doi: 10.1111/j.1749-6632.1993.tb18326.x.
Results from this study clearly indicate that Ins(1,4,5)P3 3-kinase is a target enzyme of cerebral ischemia insult. This enzyme is responsible for removal of Ins(1,4,5)P3 which, in turn, plays an important role in the maintenance of intracellular Ca2+ homeostasis. Not only did a time-dependent decrease in enzyme activity occur due to the focal cerebral ischemic insult, but there was also a second phase for the decline in enzyme activity around 6 h after the insult. Examination of the mRNA for the 3-kinase in frozen brain sections suggested an increase in message at a time (around 8 h) prior to development of tissue infarct. Since the initial decline in enzyme activity during ligation correlated well with the time for development of an infarct, assay of this enzyme could be used as a biochemical marker of cerebral ischemic insult.
本研究结果清楚地表明,肌醇(1,4,5)三磷酸3激酶是脑缺血损伤的靶酶。该酶负责去除肌醇(1,4,5)三磷酸,而肌醇(1,4,5)三磷酸反过来在维持细胞内钙离子稳态中起重要作用。由于局灶性脑缺血损伤,酶活性不仅出现了时间依赖性降低,而且在损伤后约6小时还出现了酶活性下降的第二阶段。对冰冻脑切片中3激酶的信使核糖核酸进行检测表明,在组织梗死形成之前的某个时间(约8小时)信使核糖核酸有所增加。由于结扎过程中酶活性的最初下降与梗死形成的时间密切相关,因此该酶的检测可作为脑缺血损伤的生化标志物。