Zubrow Alan B, Delivoria-Papadopoulos Maria, Ashraf Qazi M, Fritz Karen I, Mishra Om P
Department of Pediatrics, College of Medicine, Drexel University, Philadelphia, PA, USA.
Neurosci Lett. 2002 Dec 19;335(1):5-8. doi: 10.1016/s0304-3940(02)01138-2.
The present study tested the hypothesis that hypoxia results in increased Ca(2+)/calmodulin-dependent protein kinase IV (CaM kinase IV) activity and that inhibition of nitric oxide (NO) synthase by N-nitro-L-arginine (NNLA) prevents the hypoxia- induced increase in neuronal nuclear CaM kinase IV activity in newborn piglets. CaM kinase IV activity was determined in normoxic (Nx), hypoxic (Hx), and NNLA-pretreated Hx piglets. Cerebral hypoxia was confirmed biochemically. There was a significant difference between CaM kinase IV activity (pmoles/mg protein/min) in Nx (285.22+/-86.12), Hx (494.77+/-99.79, P<0.05 vs. Nx), and NNLA-pretreated Hx (249.55+/-53.85)(P=NS vs. Nx, P<0.05 vs. Hx) animals. The results demonstrate that the cerebral tissue hypoxia results in an increase in neuronal nuclear CaM kinase IV activity, and the hypoxia-induced increase in CaM kinase IV activity is NO-mediated.
缺氧会导致钙/钙调蛋白依赖性蛋白激酶IV（CaM激酶IV）活性增加，并且N-硝基-L-精氨酸（NNLA）对一氧化氮（NO）合酶的抑制作用可防止新生仔猪神经元细胞核中CaM激酶IV活性因缺氧而增加。测定了常氧（Nx）、缺氧（Hx）以及经NNLA预处理的Hx仔猪的CaM激酶IV活性。通过生化方法确认了脑缺氧情况。Nx组（285.22±86.12）、Hx组（494.77±99.79，与Nx组相比P<0.05）以及经NNLA预处理的Hx组（249.55±53.85）（与Nx组相比P=无显著差异，与Hx组相比P<0.05）动物的CaM激酶IV活性（皮摩尔/毫克蛋白/分钟）存在显著差异。结果表明，脑组织缺氧会导致神经元细胞核中CaM激酶IV活性增加，且缺氧诱导的CaM激酶IV活性增加是由NO介导的。
