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目的探讨子痫前期患者生化指标及分子机制。方法收集2011年3月至2015年12月48例子痫前期轻度患者,32例子痫前期重度患者,以及50例正常妊娠妇女血清及胎盘,检测血清中胎盘生长因子(placenta growth factor,PLGF),可溶性血管内皮生长因子受体1(soluble fms-like tyrosine kinase-1,s Flt-1)的水平,以及分析胎盘中活性氧(reactive oxygen species,ROS)与抗氧化基因的表达情况。结果在孕12~16周、孕26~30周及孕37~41周,轻度与重度组PLGF水平均显著低于正常妊娠组水平(P<0.05);在孕26~30周及孕37~41周,轻度与重度组s Flt-1水平显著高于正常妊娠组水平(P<0.05);轻度与重度组胎盘氧化应激明显增强,表现为ROS水平增加及抗氧化应激基因的上调。结论孕妇血清中PLGF和s Flt-1水平变化与子痫前期相关;ROS异常增加是子痫前期发生的分子基础。
Objective To explore the biochemical indexes and molecular mechanisms of preeclampsia. Methods The serum and placenta of 48 preeclampsia patients, 32 severe preeclampsia patients and 50 normal pregnant women were collected from March 2011 to December 2015. Serum placenta growth factor (PLGF) (SFt-1), and to analyze the expression of reactive oxygen species (ROS) and antioxidant genes in the placenta. Results The levels of PLGF in mild and severe groups were significantly lower than those in normal pregnancy group (P <0.05) at 12-16 weeks pregnant, 26-30 weeks pregnant and 37-41 weeks pregnant. ~ 41 weeks, s Flt-1 level in mild and severe group was significantly higher than that in normal pregnancy group (P <0.05); mild and severe placental oxidative stress was significantly increased, showing increased ROS levels and anti-oxidative stress genes Up. Conclusion The changes of PLGF and s Flt-1 levels in pregnant women are associated with preeclampsia. The abnormal increase of ROS is the molecular basis of preeclampsia.