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目的:探讨缺氧后新生鼠脑内阿米巴样小胶质细胞(amoeboid microglial cell,AMC)环氧合酶(cyclooxygenase-2,COX-2)的表达。方法:将新生鼠置于缺氧装置内(5%氧气,95%氮气)2 h复制缺氧模型,缺氧后随机分为3 h,24 h,3 d,7 d和14 d五个组(n=5)。每个时间点均设正常对照组(n=5)。采用绿色荧光lectin抗体标记AMC,红色荧光Cy3标记COX-2进行免疫荧光双标染色,同时也对体外培养的BV2小胶质细胞进行免疫荧光双标染色,观察正常新生鼠脑内AMC是否表达COX-2,以及缺氧后AMC表达COX-2的变化。结果:正常新生鼠脑内胼胝体的AMC表达COX-2,缺氧激活的AMC在不同时间点表达COX-2均较对照组增强。结论:缺氧激活后的AMC以前列腺素代谢途径参与了缺氧的病理变化。
Objective: To investigate the expression of cyclooxygenase-2 (COX-2) in amoebocyte microglial cells (AMC) in neonatal rats after hypoxia. Methods: The neonatal rats were placed in hypoxia device (5% oxygen, 95% nitrogen) for 2 hours to duplicate hypoxia model. After hypoxia, the rats were randomly divided into five groups: 3 h, 24 h, 3 d, 7 d and 14 d (n = 5). Normal control group was established at each time point (n = 5). The green fluorescent lectin antibody labeled AMC, red fluorescent Cy3 labeled COX-2 double immunofluorescence staining, but also on the BV2 microglial cells in vitro immunofluorescence double-stained staining to observe the normal neonatal rat brain AMC expression of COX -2, and the changes of COX-2 expression in AMC after hypoxia. Results: The AMX expression in the corpus callosum of normal neonatal rats was significantly higher than that in the control group (P <0.05). Conclusion: AMC after hypoxia is involved in the pathological changes of hypoxia with prostaglandin metabolism pathway.