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IL-6对大鼠脑缺血-再灌注后海马IL-1R的影响
引用本文:向赟,方孝俊,许晓莉,鲁雄兵,李汉仙.IL-6对大鼠脑缺血-再灌注后海马IL-1R的影响[J].江汉大学学报(自然科学版),2004,32(3):70-73,77.
作者姓名:向赟  方孝俊  许晓莉  鲁雄兵  李汉仙
作者单位:1. 江汉大学,医学与生命科学学院,湖北,武汉,430056;中国科学院,波谱学国家重点实验室,湖北,武汉,430070
2. 恩施市人民医院,神经科内科,湖北,恩施,445700
3. 江汉大学,医学与生命科学学院,湖北,武汉,430056
摘    要:目的:探讨脑缺血-再灌注损伤(brainischemiareperfusioninjury)过程中白细胞介素-6 Interleukin-6, (IL-6)对CNS中神经元保护作用的机制及其与炎前细胞因子白细胞介素-1 Interleukin-1,IL-1)之间的关系,为 (研究脑缺血-再灌注损伤的机制提供实验和相关方面的理论基础.方法:采用四动脉暂时性阻断的方法将26只Wistar大鼠制成全脑缺血-再灌注的实验动物模型,并将大鼠分成两组:即单纯的脑缺血-再灌注对照组(n= 9)以及实验组(n = 17),两组大鼠手术前2h分别经侧脑室注入10 L生理盐水和等量的IL-6,然后采用免疫组织化学方法观察缺血-再灌注过程中大鼠海马神经元白细胞介素-1受体(Interleukin-1 receptor,IL-1R)免疫反应性的变化并进行相关的统计学分析.结果:大鼠全脑缺血-再灌注4h后海马CA1、 区IL-1R免疫反应CA3性显著增加,表现为:IL-1R免疫反应阳性细胞数显著增加、着色明显加深.结论:IL-6作为一种神经保护因子在大鼠脑缺血-再灌注损伤的病理过程中,可能通过抑制CNS中神经元的炎症因子IL-1R的表达来实现其对CNS的营养和保护作用.

关 键 词:脑缺血-再灌注损伤  IL-6  海马  IL1-R
文章编号:1009-1777(2004)03-0070-04
修稿时间:2004年3月8日

Effect of Cytokines (Interleukin-6) on Interleikin-1 Receptors in the Hippocampus of Rats Following Global Brain Ischemia-reperfusion
XIANG Yun,FANG Xiao-jun,XU Xiao-li,et al..Effect of Cytokines (Interleukin-6) on Interleikin-1 Receptors in the Hippocampus of Rats Following Global Brain Ischemia-reperfusion[J].Journal of Jianghan University:Natural Sciences,2004,32(3):70-73,77.
Authors:XIANG Yun    FANG Xiao-jun  XU Xiao-li  
Institution:XIANG Yun1,2,FANG Xiao-jun3,XU Xiao-li1,et al.
Abstract:Objective: In order to explore effect of interleukin-6 (IL-6), which was regarded as a potential endogenous neuroprotective cytokine against brain ischemia-reperfusion injury, investigate the relationship between it and another interleikin (IL-1) and provide a kind of experimental and theoretic basis. Methods:After the 26 Wistar rats were divided into two groups, the control group(n = 9) and the experiment group(n = 17), their lateral ventricles were injected into the same amount of Saline and IL-6 respectively. Then they were formed into the global brain ischemia/reperfusion models by the quadri-arteries block pattern, and the IL-1R immunoreactivity of their CA1 and CA3 areas in hippocampus were observed and assayed statistically. Results: 4 h after the global brain ischemia reperfusion the IL-1R immunoreactivity of the CA1 and CA3 areas in hippocampus increased significantly, from which we can discover the more immunoreactivity positive cells and their more deeper staining. Conclusions: IL-6, as a neuroproteceive factor in the pathogenesis of the brain ischemia-reperfusion injury of the rats, may fulfill its neuroprotective function according to inhibiting the receptor of the IL-1 in CNS.
Keywords:brain ischemia reperfusion injury  IL-6  hippocampus  IL-1R
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