TROPHOBLAST AND PLACENTAL VILLOUS CORE PRODUCTION OF LIPID PEROXIDES, THROMBOXANE, AND PROSTACYCLIN IN PREECLAMPSIA
TROPHOBLAST AND PLACENTAL VILLOUS CORE PRODUCTION OF LIPID PEROXIDES, THROMBOXANE, AND PROSTACYCLIN IN PREECLAMPSIA
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DOI：
10.1210/jc.80.6.1888
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发表时间：
1995-06-01
影响因子：
5.8
通讯作者：
WANG, YP
中科院分区：
文献类型：
--
作者：
WALSH, SW;WANG, YP
先兆子痫孕妇胎盘产生的脂质过氧化物和血栓素比正常孕妇多，但前列环素比正常孕妇少。胎盘内负责这一过程的组织隔室尚不清楚。胎盘是一种异质组织，分为滋养层细胞和绒毛核心组织，绒毛核心组织由基质和血管组织组成。在这项研究中，我们确定了胎盘室负责增加生产的脂质过氧化物和血栓素先兆子痫。胎盘来自6名正常妊娠妇女和7名先兆子痫妇女。分离滋养层细胞和绒毛核心组织，并在Dulbecco改良Eagle培养基中孵育48小时。在孵育0、2、6、16、28和48 h时采集样品，并通过过氧化物当量测定法进行脂质过氧化物测定，并通过其稳定代谢物血栓烷-B-2和6-酮-前列腺素-F-1 α的RIA进行血栓烷和前列环素测定。从先兆子痫胎盘中分离的滋养层细胞产生明显更多的脂质过氧化物（孵育48小时后，1972 +/- 502 vs. 1102 +/- 335 pmol/μ g蛋白），更多血栓烷（48小时时分别为328 +/- 57和153 +/- 53 pg/μ g）和更多的前列环素（48小时时分别为50 +/- II和13 +/- 3 pg/μ g）。从先兆子痫胎盘中分离的绒毛核心组织产生了明显更多的脂质过氧化物（455 +/- 107 vs. 241 +/- 34 pmol/μ g）和更多血栓素（148 +/- 51 vs. 76 +/- 14 pg/μ g），但前列环素产生无差异（36 +/- II vs. 40 +/- 9 pg/μ g）。由于血栓素产生的增加，血栓素与前列环素的比率在先兆子痫中高于正常绒毛核心组织（6.29 us. 2.17）。比较生产不同的车厢内的胎盘表明，脂质过氧化物和血栓素主要是由滋养层细胞和基质组织，而前列环素主要是由血管tissue.We得出结论，增加胎盘生产的脂质过氧化物和血栓素先兆子痫起源于滋养层细胞和绒毛核心车厢。由于胎盘分泌过氧化脂质，滋养层细胞可能是先兆子痫妇女母体循环中过氧化脂质增加的来源。绒毛核心中血栓素与前列环素的比例增加可能是胎盘血管收缩增加的原因。
Placentas obtained from women with preeclampsia produce more lipid peroxides and more thromboxane, but less prostacyclin, than normal. The tissue compartments within the placenta that are responsible for this are not known. The placenta is a heterogeneous tissue compartmentalized into trophoblast cells and Villous core tissue that is comprised of stromal and Vascular tissue. In this study we determined the placental compartments responsible for increased production of lipid peroxides and thromboxane in preeclampsia. Placentas were obtained from six normally pregnant women and seven women with preeclampsia. Trophoblast cells and villous core tissues were isolated and incubated in Dulbecco's Modified Eagle's Medium for 48 h. Samples were collected at 0, 2, 6, 16, 28, and 48 h of incubation and analyzed spectrophotometrically for lipid peroxides by a peroxide equivalent assay and for thromboxane and prostacyclin by RIA of their stable metabolites, thromboxane-B-2 and 6-keto-prostaglandin-F-1 alpha. Trophoblast cells isolated from preeclamptic placentas produced significantly more lipid peroxides (1972 +/- 502 vs. 1102 +/- 335 pmol/mu g protein after 48 h of incubation), more thromboxane (328 +/- 57 vs. 153 +/- 53 pg/mu g at 48 h), and more prostacyclin (50 +/- II vs. 13 +/- 3 pg/mu g at 48 h, respectively) than trophoblast cells isolated from normal placentas. Villous core tissue isolated from preeclamptic placentas produced significantly more lipid peroxides (455 +/- 107 vs. 241 +/- 34 pmol/mu g) and more thromboxane (148 +/- 51 vs. 76 +/- 14 pg/mu g) than normal Villous core tissue, but there was no difference in prostacyclin production (36 +/- II vs. 40 +/- 9 pg/mu g). Because of the increase in thromboxane production, the ratio of thromboxane to prostacyclin was higher in preeclamptic than normal villous core tissue (6.29 us. 2.17). Comparison of production by different compartments within the placenta demonstrated that lipid peroxides and thromboxane were primarily produced by the trophoblast cells and stromal tissue, whereas prostacyclin was primarily produced by the Vascular tissue.We conclude that increased placental production of lipid peroxides and thromboxane in preeclampsia originates from both the trophoblast cell and the villous core compartments. As the placenta secretes lipid peroxides, the trophoblast cells could be a source of increased lipid peroxides in the maternal circulation of women with preeclampsia. The increased ratio of thromboxane to prostacyclin in the Villous core could be responsible for increased placental vasoconstriction.