Levels of oxidative stress and redox-related molecules in the placenta in preeclampsia and fetal growth restriction
Levels of oxidative stress and redox-related molecules in the placenta in preeclampsia and fetal growth restriction
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DOI：
10.1007/s00428-003-0903-2
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发表时间：
2004-01-01
期刊：
影响因子：
3.5
通讯作者：
Konishi, I
中科院分区：
文献类型：
--
作者：
Takagi, Y;Nikaido, T;Konishi, I
最近的证据表明，氧化应激参与先兆子痫的病理生理学。采用免疫组织化学和蛋白质印迹法，我们研究了氧化应激和氧化还原相关分子，如8-羟基-2 '-脱氧鸟苷（8-OHdG），4-羟基壬烯醛（4-HNE），硫氧还蛋白（TRX）和氧化还原因子-1（ref-1）在先兆子痫，宫内生长受限（IUGR），先兆子痫+ IUGR和正常妊娠胎盘中的表达。免疫组化结果显示，IUGR组8-OHdG水平明显升高（P=0.012）或先兆子痫+ IUGR（P=0.0021），而TRX表达在子痫前期组中明显增高ref-1在子痫前期组（P =0.017）、IUGR组（P = 0.016）和子痫前期+ IUGR组（P=0.0038）中的表达明显高于正常妊娠组（P=0.045）。4-HNE水平在先兆子痫或IUGR与正常妊娠之间没有显著差异。TRX和ref-1表达在正常妊娠（rho=0.52）和复杂妊娠（rho=0.43）中均观察到显著正相关。使用Western印迹，ref-1表达在复杂妊娠中倾向于高于正常妊娠（P=0.09）。这些结果表明，氧化DNA损伤增加IUGR和氧化还原功能增强先兆子痫和IUGR与正常妊娠相比。
Recent evidence suggests that oxidative stress is involved in the pathophysiology of preeclampsia. Using immunohistochemistry and Western blotting, we investigated the oxidative stress- and redox-related molecules, such as 8-hydroxy-2'-deoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), thioredoxin (TRX) and redox factor-1 (ref-1) in the placenta in preeclampsia, intrauterine growth restriction (IUGR), preeclampsia + IUGR and in normal pregnancy. Using immunohistochemistry, the level of 8-OHdG was significantly higher in IUGR (P=0.012) or preeclampsia + IUGR (P=0.0021) than in normal pregnancy, while TRX expression was significantly higher in preeclampsia (P=0.045), and ref-1 expression was significantly higher in preeclampsia (P=0.017), IUGR (P=0.016) and preeclampsia + IUGR (P=0.0038) than in normal pregnancy. The levels of 4-HNE did not differ significantly between either preeclampsia or IUGR and normal pregnancy. A significant positive correlation was observed between TRX and ref-1 expressions in both normal (rho=0.52) and complicated (rho=0.43) pregnancies. Using Western blotting, ref-1 expression tended to be higher in complicated pregnancies than in normal pregnancy (P=0.09). These results suggest that oxidative DNA damage is increased in IUGR and that redox function is enhanced in both preeclampsia and IUGR compared with normal pregnancy.