缺氧复氧性损伤对培养海马细胞ICAM 1表达影响

　　【摘要】 目的 研究缺氧复氧性损伤对培养海马细胞细胞间黏附分子-1(ICAM-1)表达影响及银信达莫的保护作用，探讨其可能的机制。方法 将SD大鼠分设正常条件培养组、单纯缺氧复氧组(HR)、缺氧复氧+银信达莫组，于缺氧1h后复氧6h，测定海马细胞ICAM-1表达水平及细胞胞浆游离钙([Ca2+]i)、一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)、丙二醛(MDA)、还原型谷胱苷肽(GSH)水平。结果 海马细胞缺氧复氧刺激时，ICAM-1蛋白质表达、[Ca2+]i和MDA均有显著增加，而SOD、GSH、NOS明显下降;银信达莫可明显改善缺氧复氧性海马细胞ICAM-1的表达和MDA、[Ca2+]i超载增高的程度以及SOD、GSH、NOS下降程度。结论 海马细胞缺氧复氧通过直接或间接激活ICAM-1引起细胞损伤，但钙超载、氧自由基和NOS系统也共同参与了缺氧复氧性损伤。银信达莫通过直接或间接抑制上述各系统而达到减轻缺氧复氧性损伤。

　　【关键词】 一氧化氮合酶(NOS);海马细胞;细胞间黏附分子1;银信达莫

　　The effects of hypoxia reoxygenation induced injury on the expression of ICAM-1 in hippocampal neuron cells in culture and the protective function of YinXinDaMo

　　GU Jian-jun, GAO Guang-zhong, LU Jun, ZHANG Qin, JIANG Lin, LIU Xiao-xing, WANG Xiao-lin, YIN Rong-jian, YIN Chun

　　(Department of Neurosurgery, Taizhou People s Hospital Affiliated to Nantong University, Taizhou, Jiangsu 225300, China)

　　Abstract: Objective To investigate injury induced by hypoxia reoxygenation impacts on the expression of ICAM-1 in hippocampal neuron cells in culture and the protective function of YinXinDaMo. Methods The SD rats were allocated to a normal culture group, hypoxia reoxygenation alone group (HR group), a hypoxia reoxygenation+YinXinDaMo group, 6-hour reoxygenation following 1-hour hypoxia. The measurements of ICAM-1 levels, cytoplasmic free calcium ([Ca2+]i), nitric oxide synthase (NOS), superoxide dismutase (SOD), malonyl dialdehyde (MDA) and reduced glutatione form (GSH) were recorded. Results When stimulated by hypoxia reoxygenation, the elevated levels of ICAM-1, [Ca2+]i and MDA were obtained in hippocampal neuron cells, and SOD, GSH, NOS decreased significantly. YinXinDaMo could obviously improve the expression of ICAM-1 in hippocampal neuron cells with hypoxia reoxygenation, and also could inhibit the MDA, [Ca2+]i overload and the decrease of SOD, GSH, NOS. Conclusion Hypoxia reoxygenation directly or indirectly activated ICAM-1 to induce hippocampal neuron ce

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