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探讨宫内窘迫胎鼠肾组织COX-2基因表达的动态变化及其与病理改变的关系。建立胎鼠宫内缺血/再灌注动物模型、应用既染色及RT-PCR方法,观察不同程度、不同时间胎鼠宫内缺血-再灌注后胎肾组织的病理改变及COX-2mRNA表达的变化。结果显示:宫内缺血10分钟不同时间再灌注后,胎肾组织仅表现肾浊肿,COX-2mRNA表达无显著变化。而宫内缺血30分钟,再灌注6小时,胎肾近曲小管出现片状坏死,COX-2mRNA表达以6～12小时达高峰,与病理改变趋于一致。提示:前列腺素代谢在宫内窘迫胎鼠肾损伤发病过程中具有重要作用,COX-2可能作为重要介质参与新生儿肾损伤的发病过程。
To investigate the dynamic changes of COX-2 gene expression in fetal rat renal tissue and its relationship with pathological changes. The animal model of fetal intrauterine ischemia / reperfusion was established. Both the pathological changes of fetal kidney tissue and the expression of COX-2 mRNA in fetal rat after intrauterine ischemia / reperfusion were observed by both staining and RT-PCR Variety. The results showed that after intrauterine ischemia for 10 minutes, reperfused renal tissue showed renal turbidity and no significant change in COX-2 mRNA expression. The intrauterine ischemia for 30 minutes, 6 hours after reperfusion, tubular necrosis of proximal tubules, COX-2 mRNA expression reached its peak in 6 to 12 hours, consistent with the pathological changes. It is suggested that prostaglandin metabolism plays an important role in the pathogenesis of intrauterine fetal distress fetal kidney injury. COX-2 may play an important role in the pathogenesis of neonatal renal injury.