宫内窘迫胎鼠肾组织COX-2基因表达

COX-2 GENE EXPRESSION IN INTRAUTERINE DEPRESSED FETAL RAT RE- NAL TISSUE

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 explore the dynamics changes of COX-2mRNA expression in the fetal rat kidneys of intrauterine ischemia and reperfusion and relation with pathology changes, establishing the model of intrauterine ischemia and reperfusion in fetal rat. Using HE staining and RT-PCR methodes, observe pathology changes and COX-2mRNA expression in fetal rat kidneys of ischemic and reperfusion with different dregree and different time. Results showed fetal kidneys tissues only revealed cloudy swelling, there was no change in COX-2mRNA expression at 10 minutes of ischemia groups. However, in 30 minutes of ischemia groups, proximal tubules revealed patchy necrosis, COX-2mRNA expression increased with reperfusion prolonged and was at its highest in 6 ~ 12 hours. Thesefore, prostglandins metabolism may play an important role in the kidney injure in fetal rats of intrauterine ischemia. COX-2 may take part in the mechanism of neonatal kidney injure as an important mediator.