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目的为探讨ＨＩＢＤ发病机制方法制备左脑缺氧缺血性脑损伤（ＨＩＢＤ）的新生大鼠模型，用ＩＬ１β寡核苷酸探针，通过ＤＮＡＲＮＡ斑点杂交技术，检测ＨＩＢＤ后海马、皮质不同时间ＩＬ１β及ｍＲＮＡ。结果斑点杂交技术敏感特异，最低可检出１ｐｇ总ＲＮＡ，且ＩＬ１β寡核苷酸探针只能特异地与其相应核酸杂交。ＨＩＢＤ后１小时ｍＲＮＡ水平开始增高，３小时为高峰表达，１２小时基本消失。其海马表达略高于皮质。结论ＩＬ１β转录水平表达在ＨＩＢＤ后早期出现，其作用可能与ＨＩＢＤ发病过程的炎性过程有关。
Objective To investigate the mechanism of HIBD pathogenesis of neonatal rat model of hypoxic-ischemic brain damage (HIBD), using IL 1β oligonucleotide probe by DNA dot blot hybridization detection of HIBD hippocampus, Cortical IL 1β and mRNA at different times. Results Dot blot hybridization technology is sensitive and specific, the lowest detectable 1pg of total RNA, and IL 1β oligonucleotide probe can only specifically hybridize with its corresponding nucleic acid. HIBD 1 hour after the mRNA level began to rise, 3 hours for peak expression, 12 hours basically disappeared. The hippocampus expressed slightly higher than the cortex. Conclusions The expression of IL-1β in the early stage of HIBD may play an important role in the pathogenesis of HIBD.