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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。
Objective To study the effect of hypoxia-reoxygenation injury on the expression of intercellular adhesion molecule-1 (ICAM-1) in hippocampus and the protective effect of silver cysteamine, and to explore its possible mechanism. Methods SD rats were divided into normal culture group, pure hypoxia-reoxygenation group (HR), hypoxia-reoxygenation + silver cedutamide group, reoxygenation for 6 hours after hypoxia 1h, and the expression level of ICAM-1 in hippocampal cells (Ca2 +) i, NOS, SOD, MDA and GSH levels in the cytoplasm were measured. Results When hippocampal cells were stimulated by hypoxia / reoxygenation, the protein expression of [Ca2 +] i and ICAM-1 in hippocampus were significantly increased, while the contents of SOD, GSH and NOS in hippocampus were significantly decreased. The expression of ICAM-1 and MDA [, Ca2 +] i increased the degree of overload and SOD, GSH, NOS decreased. Conclusion Hypoxia / reoxygenation in hippocampal cells can induce cell injury by directly or indirectly activating ICAM-1. However, calcium overload, oxygen free radicals and NOS system also participate in hypoxia-reoxygenation injury. Silver letter Damo through direct or indirect inhibition of the above systems to achieve and reduce hypoxia and reoxygenation injury.