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目的 缺血缺氧性肾损伤是一个复杂的病理生理过程,炎症反应在其中占有重要的作用。该文 旨在观察宫内窘迫后胎鼠肾组织炎症介质环氧化酶 2(COX 2)蛋白和基因表达及其代谢产物前列环素I2(PGI2), 前列腺素E2(PGE2)和血栓素(TXA2)的动态变化,初步探讨COX 2在宫内窘迫胎鼠肾损伤发病机制中的作用。方 法 制备胎鼠宫内缺血缺氧再灌注模型(缺血缺氧组:缺血缺氧30min;再灌注组:缺血缺氧30min后,分别再灌注 0.5h,2h,6h,12h,24hand30h)。各时间点分别取胎鼠20只,假手术组胎鼠22只,将肾组织匀浆后采用 RT PCR,Western印迹杂交和放免法进行检测。同时苏木精 伊红染色观察肾组织病理学改变。结果 宫内窘迫 后胎肾组织COX 2蛋白和基因表达上调,PGI2的稳定代谢产物6 keto PGF1α及PGE2均于再灌注2h开始增高(P <0.05)。其中6 keto PGF1α增加迅速,于再灌注12h达高峰(P<0.01),PGE2于再灌注24h达最高水平(P< 0.01),而TXB2增加幅度不大。结论 宫内缺血再灌注从转录水平诱导胎肾COX 2蛋白表达增强,COX 2的主要 代谢产物是PGI2和PGE2。COX 2可能通过PGI2和PGE2对缺血性胎肾损伤具有保护作用,因此,在围产期肾损 伤不宜应用COX 2抑制剂。
Objective Ischemic and hypoxic renal injury is a complex pathophysiological process in which inflammatory response plays an important role. The aim of this study was to observe the protein and gene expression of cyclooxygenase 2 (COX-2) and its metabolites PGI2, PGE2 and thromboxane in fetal rat renal tissue after intrauterine distress TXA2) dynamic changes, preliminary study of the role of COX 2 in the pathogenesis of fetal renal injury in fetal distress. Methods The intrauterine ischemia / reperfusion model was established by intrauterine ischemia (hypoxia / hypoxia group: ischemia / hypoxia for 30 min; reperfusion group: hypoxia for 30 min followed by reperfusion for 0.5 h, 2 h, 6 h, 12 h, 24 h ). At each time point, 20 fetuses and 22 fetuses were sacrificed. The kidneys were homogenized and tested by RT PCR, Western blotting and radioimmunoassay. At the same time hematoxylin and eosin staining pathological changes in renal tissue. Results The mRNA and protein expression of COX-2 in fetal kidney increased after intrauterine distress. The steady-state metabolites of 6-keto-PGF1α and PGE2 in PGI2 increased at 2 hours after reperfusion (P <0.05). Among them, 6 keto PGF1α increased rapidly, reaching the peak at 12h after reperfusion (P <0.01), PGE2 reached the highest level at 24h after reperfusion (P <0.01), while the increase of TXB2 was not significant. Conclusion Intrauterine ischemia-reperfusion induced the expression of COX 2 protein in fetal kidney from transcriptional level. The main metabolites of COX 2 are PGI2 and PGE2. COX 2 may have protective effects on ischemic fetal kidney injury through PGI2 and PGE2. Therefore, COX 2 inhibitors should not be used during perinatal kidney injury.