摘要
目的观察妊娠期糖尿病(GDM)产妇胎盘组织内质网应激(ERS)发生情况并探讨其对胎盘组织形态学的影响。方法 GDM产妇(GDM组)和健康产妇(对照组)各30例,分娩时收集胎盘组织,Western blot法检测胎盘组织中的磷酸化蛋白激酶R样内质网激酶(p-PERK)、CCAAT/增强子结合蛋白同源蛋白(CHOP)。HE染色对胎盘组织行病理学观察。结果 GDM组p-PERK、CHOP相对表达量均高于对照组(P均<0.05)。病理检查显示,GDM组胎盘组织出现绒毛成熟不良、干绒毛小动脉管壁增厚及管腔狭窄、合体细胞结节增多、绒毛间质内毛细血管过度充盈、细胞滋养叶细胞及血管合体膜形成增加的例数高于对照组(P均<0.05)。GDM组胎盘组织中p-PERK、CHOP表达与胎盘组织异常形态学改变呈正相关关系(r分别为0.359、0.366,P均<0.05)。结论 GDM产妇胎盘组织呈ERS状态,其与产妇胎盘组织异常形态学改变有关。
Objective To investigate the ralationship between endoplasmic reticulum stress ( ERS ) and damage of histomorphology of placentas in gestational diabetes mellitus (GDM).Methods Thirty women with GDM(GDM group) and 30 normal pregnan women ( control group ) were included in this study .Placentas of all women in two groups were col-lected during the delivery .The expression of phosphorylated protein kinase R-like ER kinase ( p-PERK) and CCAAT/en-hancer-binding protein homologous protein ( CHOP ) in two groups were deteced by western blot method .The features of placentas pathologicchanges were observed by using microscopy .Results The expression phosphorylated PERK and CHOP protein were significantly increased in GDM group as compared with the control group (all P〈0.05).Placentas obtained from GDM group had immature villi , thickening of trunk villus small artery wall , narrowing of lumen , increasing number of syncytial sprouts , the interstitial blood capillary expanding and engorge , proliferating cytotrophoblasts and thickening of vas-culo-syncytial membrane under light microscopy .Placentas from control group did not show the pathologic changes as men-tioned above.Bivariate analysis showed that lymphatic p-PERK and CHOP expression were positively correlated with the damage of histomorphology of placentas in GDM (r=0.359, 0.366, respectively,all P〈0.05).Conclusion ERS was overexpressed in placental tissue of DGM and may be positive related with the damage of histomorphology of the placentas .
出处
《山东医药》
CAS
2014年第30期23-25,共3页
Shandong Medical Journal
关键词
妊娠期糖尿病
胎盘
内质网应激
蛋白激酶R样内质网激酶
CCAAT/增强子结合蛋白同源蛋白
gestational diabetes mellitus
placenta
endoplasmic reticulum stress
phosphorylated protein kinase r-like ER kinase
CCAAT/enhancer-binding protein homologous protein