论文部分内容阅读
目的探讨妊娠高血压疾病子痫前期患者胎盘中HO-2及TNF-α表达及其与妊高病发病机制之间的关系。方法采用免疫组织化学方法测定24例子痫患者和24例正常妊娠妇女(对照组)胎盘中HO-2、TNF-α表达水平,并分析两者相关性。结果 1.HO-2主要表达于血管内皮细胞、平滑肌细胞胞浆及胞膜上、而滋养细胞及间质细胞中表达较少。且HO-2在轻度及重度子痫前期患者表达均低于正常妊娠妇女,两者分别与正常晚孕组比较,轻度子痫前期与正常对照组相比差别无显著性,而重度子痫前期与正常对照组比较,差别有显著性。2.TNF-α主要表达于滋养细胞、血管内皮细胞胞膜中,而间质细胞内表达最少。且TNF-α在轻度及重度子痫前期患者表达均低于正常妊娠妇女,两者分别与正常晚孕组比较,差别均有显著性。3.正常组、PIH组HO-2及TNF-α存在负相关关系(r=-0.536、-0.574)。结论 HO-2可能是胎盘血管内皮细胞的保护性因素,而TNF-α可能引起胎盘血管内皮细胞损伤,可导致血管调节因子失衡,两者存在负相关关系,在妊高病发病过程中起一定作用。
Objective To investigate the relationship between the expression of HO-2 and TNF-α in the placenta and the pathogenesis of pregnancy induced hypertension in patients with pregnancy induced hypertension (BPH). Methods The expression of HO-2 and TNF-α in placenta of 24 patients with eclampsia and 24 normal pregnant women (control group) were detected by immunohistochemistry. The correlation between them was analyzed. HO-2 is mainly expressed in the vascular endothelial cells, smooth muscle cells in the cytoplasm and membrane, while less in trophoblastic and interstitial cells. The expression of HO-2 in patients with mild and severe preeclampsia was lower than that in normal pregnant women. There was no significant difference between mild preeclampsia and normal control group, The difference between preeclampsia and normal control group was significant. 2.TNF-α is mainly expressed in the membrane of trophoblasts and vascular endothelial cells, while stromal cells express the least. The expression of TNF-α in patients with mild and severe preeclampsia was lower than that in normal pregnant women, both of which were significantly different from those in normal pregnancy group. There was a negative correlation between HO-2 and TNF-αin the PIH group (r = -0.536, -0.574). Conclusions HO-2 may be a protective factor in placental vascular endothelial cells. TNF-α may cause placental vascular endothelial cell injury, which may lead to imbalance of angio regulatory factors. There is a negative correlation between HO-2 and placental vascular endothelial cells, which may play a role in the pathogenesis of PIH effect.