Hwang In Koo, Yoo Ki-Yeon, Kim Dae Won, Lee Hak-Ju, Kang Ha-Young, Lee Hyeon-Yong, Kang Tae-Cheon, Choi Soo Young, Kim Yong-Sun, Won Moo Ho
Department of Anatomy, College of Medicine, Hallym University, Chunchon 200-702, South Korea.
Department of Biomedical Sciences and Research Institute for Bioscience and Biotechnology, Hallym University, Chunchon 200-702, South Korea.
Brain Res. 2006 Aug 23;1106(1):197-204. doi: 10.1016/j.brainres.2006.05.098. Epub 2006 Jul 11.
Interlukin-2 (IL-2) is an important cytokine in the brain: IL-2 and its receptors are involved with inflammatory processes. Chronological changes in IL-2 level in serum, and IL-2 and its receptor (IL-2 receptor beta, IL-2Rbeta) immunoreactivities and levels were examined in the hippocampal CA1 region after transient forebrain ischemia in gerbils. IL-2 level in serum significantly decreased 12 h after ischemia/reperfusion. IL-2 immunoreactivity was detected in the somata of pyramidal cells in sham-operated group. At 15 min after ischemia, IL-2 immunoreactivity was shown in non-pyramidal cells as well as pyramidal cells. One day after ischemia, IL-2 immunoreactivity was lowest, and IL-2 immunoreactivity is shown in non-pyramidal cells from 2 days after ischemia. Four days after ischemia, IL-2 immunoreactivity was shown in dying pyramidal cells. IL-2Rbeta immunoreactivity in the sham-operated and 15 min-3 min post-ischemic groups is detected in the cell membrane of pyramidal cells. From 3 h after ischemia, IL-2Rbeta immunoreactivity is found in cytoplasm and nuclei, but not in cell membrane. IL-2Rbeta immunoreactivity decreases from 6 h after ischemia and is shown mainly in non-pyramidal cells from 3 days after ischemia. The data of Western blot analyses for IL-2 and IL-2Rbeta was similar to the immunohistochemical data. IL-2 infusion into cerebrospinal fluid did not protect hippocampal neurons from ischemic damage. These results suggest that IL-2 and IL-2Rbeta show malfunction from 3 h after ischemia, and exogenous IL-2 does not protect ischemic neuronal damage.
白细胞介素-2(IL-2)是大脑中的一种重要细胞因子:IL-2及其受体参与炎症过程。在沙土鼠短暂性前脑缺血后,检测了海马CA1区血清中IL-2水平以及IL-2及其受体(IL-2受体β,IL-2Rβ)的免疫反应性和水平随时间的变化。缺血/再灌注12小时后,血清中IL-2水平显著降低。在假手术组的锥体细胞胞体中检测到IL-2免疫反应性。缺血15分钟后,非锥体细胞以及锥体细胞中均显示出IL-2免疫反应性。缺血1天后,IL-2免疫反应性最低,缺血2天后非锥体细胞中显示出IL-2免疫反应性。缺血4天后,垂死的锥体细胞中显示出IL-2免疫反应性。在假手术组以及缺血后15分钟至3分钟组的锥体细胞细胞膜中检测到IL-2Rβ免疫反应性。缺血3小时后,在细胞质和细胞核中发现IL-2Rβ免疫反应性,但细胞膜中未发现。缺血6小时后,IL-2Rβ免疫反应性降低,缺血3天后主要在非锥体细胞中显示。IL-2和IL-2Rβ的蛋白质印迹分析数据与免疫组织化学数据相似。向脑脊液中注入IL-2并不能保护海马神经元免受缺血损伤。这些结果表明,缺血3小时后IL-2和IL-2Rβ出现功能异常,外源性IL-2不能保护缺血性神经元损伤。