国际妇产科学杂志 ›› 2014, Vol. 41 ›› Issue (4): 443-447.

• 综述 • 上一篇    下一篇

脱落滋养细胞在子痫前期发病机制中的作用

沈方,陈奇,肖建平   

  1. 200011 上海,复旦大学附属妇产科医院(沈方,陈奇);南京医科大学附属无锡市妇幼保健院产前诊断中心(陈奇,肖建平);新西兰奥克兰大学妇产科学系(陈奇)
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2014-08-15 发布日期:2014-08-15
  • 通讯作者: 肖建平

The Role of Trophoblastic Debris in the Pathogenesis of Preeclampsia

SHEN Fang, CHEN Qi , XIAO Jian-ping   

  1. Obstetrics and Gynaecology Hospital of Fudan University, Shanghai 200011,China(SHEN Fang, CHEN Qi);Prenatal Diagnosis Center,Wuxi Maternity and Child Health Hospital Affiliated Nanjing Medical University, Wuxi 214002,China(CHEN Qi , XIAO Jian-ping);Department of Obstetrics and Gynaecology, the University of Auckland, New Zealand(CHEN Qi)
  • Received:1900-01-01 Revised:1900-01-01 Published:2014-08-15 Online:2014-08-15
  • Contact: XIAO Jian-ping

摘要: 子痫前期是妊娠期特有疾病,其特征为系统性血管内皮细胞活化和过度的炎症反应。尽管子痫前期的发病机制尚不明确,但是某些胎盘因素和母体因素参与子痫前期的发病机制的学说得到了普遍的认可。脱落滋养细胞是参与子痫前期发病的胎盘因素之一。正常妊娠过程中,从妊娠6周起,滋养细胞以凋亡的形式从胎盘脱落进入母体血液循环,并被阻滞在肺血管内。子痫前期患者脱落滋养细胞的数量增加,1893年就有学者提出,脱落滋养细胞参与了子痫前期的发病过程。近期研究显示,血管内皮细胞在吞噬坏死脱落滋养细胞后发生活化,这种血管内皮细胞的异常常见于子痫前期患者。有很多可能的因素会促使滋养细胞在脱落过程中从凋亡形式变为坏死形式,其中抗磷脂抗体、炎性细胞因子如白细胞介素6(IL-6)、转化生长因子β1(TGF-β1)和子宫螺旋动脉重铸不良发挥重要作用。目前,子痫前期尚无有效的治疗方法,但是妊娠妇女补钙和增加维生素C的摄入可以保护血管内皮细胞在吞噬坏死脱落滋养细胞后不被活化,从而降低子痫前期发病的风险。

关键词: 滋养层, 先兆子痫, 内皮

Abstract: Preeclampsia is a pregnancy specific complication which is characterized by systemic endothelial cell activation and exaggerated inflammatory response. Although the pathogenesis of preeclampsia is unclear,it is well recognized that placental factor(s) and maternal factor(s) contribute to the pathogenesis of preeclampsia. Trophoblastic debris shed from placenta is one of the possible placental factors. During the pregnancy, trophoblastic debris is shed into the maternal blood to become trapped against the maternal pulmonary endothelium as early as 6 weeks of gestation in an apoptosis form. Trophoblastic debris was reported to be involved in the pathogenesis of preeclampsia in 1893. The increased amount of trophoblastic debris is seen in preeclampsia. Recent study showed that phagocytosis of necrotic trophoblastic debris results in endothelial cell activation that seen in preeclampsia. There are many potential factors that could switch apoptotic trophoblastic debris into necrotic trophoblastic debris. Of them, antiphospholid antibodies, inflammatory cytokines like IL-6, TGF-β1 and failure of spiral artery transformation play an important role on it. To date even there is no effective treatment on preeclampsia, calcium and vitamin C supplementation may reduce the risk for developing preeclampsia through preventing endothelial cell activation induced by phagocytosis of necrotic trophoblastic debris.

Key words: Trophoblasts, Pre-eclampsia, Endothelial cells