摘要
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 amoeboid microglial cell（ AM C ）in the neonatal rat brain after hypoxia. Methods：The hypoxic models in the neonatal rats were prepared by the hypoxic e- quipment（5% O2 ,95% N2）for 2 hours. The rats were randomized into 3 h,24 h,3 d,7 d and 14 d（n =5 for each time point） groups after hypoxia. One normal group（ n = 5 ）was used as control. To observe the expression of COX-2 in AMC and the effect of hypoxia on the expression of COX-2 in AMC, the double-immunofluorescenee staining was used with AMC labeled by green fluoreseenee-lectin and COX-2 by red fluorescence Cy3. The double-stain was also applied to BV2 cells cultured in vitro. Results：The expression of COX-2 in AMC was detected in the corpus callosum of neonatal rat brain. After AMC was activated by hypoxia, the COX-2 expression increased significantly at different time points when compared with the control group. Conclusion：Activated AMC after hypoxia was involved in pathophysiologic process of hypoxia through prostaglandin metabolic pathway.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2014年第1期55-59,共5页
Chinese Journal of Neuroanatomy
基金
国家自然科学基金(31100769)
