| 缺氧抑制脑动脉Kv2.1通道作用机制的研究 |
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| 引用本文： | 朱雨岚,陈莉,朱延梅,孙威,李倩. 缺氧抑制脑动脉Kv2.1通道作用机制的研究[J]. 中风与神经疾病杂志, 2010, 27(1) |
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| 作者姓名： | 朱雨岚 陈莉 朱延梅 孙威 李倩 |
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| 作者单位： | 1. 哈尔滨医科大学附属第二医院神经内科,黑龙江,哈尔滨,150086
2. 哈尔滨医科大学药学院,黑龙江,哈尔滨,150086 |
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| 基金项目： | 国家自然科学基金资助项目(30670729); 院博士启动基金(BS2006-12); 黑龙江省博士后基金课题(LBH-Z06244) |
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| 摘 要： | 目的探讨缺氧对脑动脉Kv通道抑制作用的机制是否由内源性15-羟二十碳四烯酸(15-HETE)介导。方法选取健康Wistar大鼠,通过酶法分离培养脑动脉和颈内动脉平滑肌细胞,分为正常对照组、缺氧组和去甲二氢愈创木酸(NDGA)缺氧组,正常对照组平滑肌细胞常规培养48h、缺氧组在缺氧箱内培养48h、NDGA缺氧组加入50μmol/L的NDGA后在缺氧箱内培养48h,使用RT-PCR和Western blotting技术检测大鼠脑动脉和颈内动脉平滑肌细胞上Kv2.1通道mRNA及蛋白质的表达情况。结果缺氧可以抑制大鼠脑动脉和颈内动脉平滑肌细胞上Kv2.1通道的表达,缺氧组与正常对照组相比,Kv2.1通道mRNA及蛋白质的表达下调(P<0.05);采用NDGA抑制15-脂氧化酶(15-LOX)后,导致脑动脉和颈内动脉平滑肌细胞上Kv2.1通道的表达上调,NDGA可以保护缺氧对于Kv通道的抑制,NDGA缺氧组与缺氧组相比,Kv2.1通道mRNA及蛋白质的表达明显上调(P<0.05)。结论缺氧可能通过内源性15-HETE发挥对Kv通道的抑制作用,15-HETE可能是影响脑动脉张力的重要中介因素。
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| 关 键 词： | 缺氧 NDGA 15-脂氧化酶 15-HETE Kv2.1 |
The mechanism study of inhibition of hypoxia on the expression of Kv2.1 channel in cerebral arteries |
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| ZHU Yu-lan,CHEN Li,ZHU Yan-mei,et al.. The mechanism study of inhibition of hypoxia on the expression of Kv2.1 channel in cerebral arteries[J]. Journal of Apoplexy and Nervous Diseases, 2010, 27(1) |
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| Authors: | ZHU Yu-lan CHEN Li ZHU Yan-mei et al. |
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| Affiliation: | ZHU Yu-lan,CHEN Li,ZHU Yan-mei,et al.(Department of Neurology,The 2nd Affiliated Hospital of Harbin Medical University,Harbin 150086,China) |
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| Abstract: | Objective To reveal whether hypoxia could inhibit the expression of Kv channel in cerebral artery through the endogenous 15-hydroxyeicosatetraenoic acid(15-HETE)way.Methods Smooth muscle cells originated from the cerebral artery and internal carotid artery of Wistar rats were seperated and cultured by enzyme digestion method.The cells were then assigned randomly into three groups:control group,hypoxia group and Nordihydro-guiairetic acid(NDGA)hypoxia group.The expression of Kv2.1 channel mRNA and protein in... |
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| Keywords: | Hypoxia NDGA 15-Lipoxygenase 15-HETE Kv2.1 |
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