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

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF PERINATAL MEDICINE
Issue:
1
DOI:
10.3760/cma.j.issn.1007-9408.2009.01.005
Key Word:
先兆子(癎);PPARγ;肿瘤坏死因子α;免疫组织化学;Preeclampsia;PPAR gamma;Tumor necrosis factor-alpha;Immunohistochamistry

Abstract´╝Ü Objective To investigate the expression of peroxisome proliferators-activated receptorgamma,PPARγ)and tumor necrosis factor-α(TNF-α)in human placental tissues and to discuss the role of PPARγ and 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 PPAR7 and TNF-αwere 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 PPARγ between SPE and controls,moreover,the expression of TNF-α was dramatically increased in SPE than in controls(P<0.05).PPARγ/TNF-α 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 PPARγ and TNF-α.Conclusions The decrease of PPAR-γ/TNF-α ratio may be related to the pathological changes of late-onset precclampsia 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.

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