Abstract：Objective To examine the mRNA and protein expressions of cyclooxygenase-2 (COX-2) and the kinetic changes of three metabolites (PGI 2, PGE 2 and TXA 2) of COX-2 in kidney tissues of fetal rats after intrauterine distress (ID), and to explore the possible roles of COX-2 in the pathogenesis of kidney impairment of fetal rats after ID. Methods A model of intrauterine ischemia and hypoxia of fetal rats was made by occluding one side of vessels supplying two horn uteri. The fetal rats in the other side were used as Sham-operation group (n=22). After 30 minutes of blood occlusion, reperfusion started. Pups were removed 0, 0.5, 2, 6, 12, 24 and 30 hrs post-reperfusion respectively (n=20 for each time point). After the renal tissues of fetal rats were homogenized, RT-PCR, Western blotting and radioimmunoassay methods were used to detect the mRNA and protein expressions of COX-2 and the kinetic changes of PGI 2, PGE 2 and TXA 2 concentrations. At the same time, hematoxylin-eosin staining was used to observe the histopathological changes of the kidney.Results After intrauterine ischemia, hypoxia and reperfusion, the expressions of COX-2 protein and gene in fetal rat kidney were significantly up-regulated. Compared with the Sham-operation group, the concentrations of 6-keto-PGF 1α and PGE 2 began to increase following 2 hrs of reperfusion, and reached a peak 12 hrs and 24 hrs after reperfusion respectively. The TXB 2 concentration in the Ischemia-reperfusion group was not different from the Sham-operation group at any reperfusion time point.Conclusions Intrauterine ischemia, hypoxia and reperfusion can induce the up-regulation of COX-2 expression in fetal kidney at the transcriptional level. COX-2 may play a protective role in ischemic impairment of fetal kidney through PGI 2 and PGE 2. It is suggested that COX-2 inhibitors should not be used for kidney impairment patients during the perinatal period.
TENG Yue-E,HU Xiao-Bin,WEI Ke-Lun. Expression of cyclooxygenase-2 in the kidney of fetal rats following intrauterine distress
[J]. CJCP, 2005, 7(1): 15-19.
