过氧化物酶体增殖物激活受体-γ与肿瘤坏死因子-α在重度子痫前期发病中相互作用的探讨  

Interaction between peroxisome proliferator-activated receptor-gamma and tumor necrosis factor-alpha in pathogenesis of severe preeelampsia

作　　者：王伽略[1] 杨孜[1] 王荣[1] 朱锦明[1] 

机构地区：[1]北京大学第三医院妇产科,100083

出　　处：《中华围产医学杂志》2009年第1期15-19,共5页Chinese Journal of Perinatal Medicine

基　　金：国家自然科学基金面上项目（30471821）和首都医学科学发展基金（2002-3031）

摘　　要：目的探讨过氧化物酶体增殖物激活受体-γ（peroxisome proliferator-activated receptor-gamma，PPAR-γ）与肿瘤坏死因子-α（tumor necrosis factor-alpha，TNF-α）在重度子痫前期发病中的作用及相互关系。方法采用免疫组织化学SP法，检测68例不同发病时间的重度子痫前期伴或不伴肝损害者胎盘组织PPAR-γ与TNF-α的表达，并与54例早、中、晚孕期正常妊娠绒毛或胎盘组织比较。结果两组孕妇胎盘组织均有PPAR-γ与TNF-α的表达。正常妊娠中期和妊娠28～32周胎盘PPAR-γ表达明显低于妊娠早期（12．03±6．38，11．17±3．57和18．46±5．27，P〈0．05）；TNR-α在正常妊娠早期胎盘表达强度高于中期和晚期各组（P〈0．05）。PPAR-γ／TNF-α比值在正常妊娠各不同孕期组间差异无统计学意义。不同发病孕周的重度子痫前期组与正常妊娠组比较，TNF-α表达明显升高（P均〈0．05）；发病孕周〈32周的重度子痫前期组与正常妊娠组比较，PPAR-γ／TNF-α比值差异无统计学意义（P〈0．05），发病孕周为32～周和〉34周两组中，伴或不伴肝损害者PPAR-γ／TNF-α比值均明显低于正常妊娠者（P〈0．05）。正常妊娠和重度子痫前期组内PPAR-γ与TNF-α之间未见直线相关性（正常妊娠组，r=0．227，P=0．125；重度子痫前期组r=0．142，P=0．267）。结论晚发型重度子痫前期孕妇胎盘PPAR-γ／TNF-α比值下降可能与较晚发生的子痫前期病理变化有关，其在重度子痫前期发生发展中复杂的相互作用及调节机制还有待深入研究。Objective To investigate the expression of peroxisome proliferators-activated receptorgamma, PPARγ） and tumor necrosis factor-α （TNF-γ） in human placental tissues and to discuss the role of PPARγand TNF-α in the pathogenesis of severe preeclampsia（SPE）. Methods Placenta tissues were obtained from 70 cases of SPE with the onset at different gestations with or without liver impairement. Another 54 placental or villi samples from normal pregnancy at the first, second and third trimester were collected as controls. The protein expression of PPARγ and TNF-α were determined by immunohistochemistry. Results Both PPARγ and TNF-α were detected in placentas in all subjects. Among the controls, the expressions of PPARγ in the second trimester and 28-32 weeks of gestation were much lower than that in the first trimester （12.03± 6.38 and 11.17 ± 3.57 vs 18. 46 ± 5.27, P〈 0. 05）, while the TNF-α expressions in the second and third trimester were much lower than that in the first （P〈 0. 05）. No significant difference in PPARγ/TNF-α ratios was detected among the three trimesters in normal pregnancy. There was no difference on the expression of PPARγbetween SPE and controls, moreover, the expression of TNF-α was dramatically increased in SPE than in controls （P〈0.05）. PPARγ/TNFα ratio in SPE women with the onset 〈32 weeks was much lower than in the controls （P〈0.05）. Neither group showed linear correlation between the expression of PPARγand TNF-α. Conclusions The decrease of PPAR-γ/TNF-α ratio may be related to the pathological changes of late-onset preeclampsia and secondary to maternal systemic damage. The none linear correlation between PPARγ and TNF-α expression and their interactions in the pathogenesis of SPE warrants further researches.

关 键 词：先兆子痫 PPARΓ 肿瘤坏死因子Α 免疫组织化学 

分 类 号：R714[医药卫生—妇产科学]