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目的探讨人类主要组织相容性抗原G(HLA G) mRNA在特发性胎儿生长受限(IFGR)产妇胎盘组织中的表达及其与IFGR发病的关系。方法采用原位杂交法,检测20例IFGR产妇(IFGR组)及28例正常产妇(对照组)胎盘组织中HLA GmRNA的表达水平和表达部位,并对两组产妇的胎盘组织进行病理学观察。结果( 1 )IFGR组产妇胎盘出现病理改变的发生率为75%(15 /20), 主要为慢性绒毛膜炎、胎盘梗死及绒毛发育迟缓;明显高于对照组的18% (5 /28),两组比较,差异有统计学意义(P=0 001)。(2)IFGR组产妇胎盘HLA GmRNA的阳性表达率为45% ( 9 /20),明显低于对照组的79% ( 22 /28 )。两组比较,差异有统计学意义(P= 0 017 )。( 3 )HLA GmRNA的阳性表达部位主要位于胎盘绒毛外细胞滋养细胞及合体滋养细胞的细胞质内,呈紫蓝色的颗粒状沉淀,轮廓清晰。(4)HLA GmRNA表达阴性者,出现胎盘病理改变的例数较HLA GmRNA表达阳性者明显增多(r=-0 638,P=0 008 )。结论IFGR产妇胎盘组织中HLA GmRNA表达水平明显下降,HLA GmRNA的异常表达可能参与了IFGR的发病过程。
Objective To investigate the expression of human major histocompatibility antigen G (HLA G) mRNA in the placenta of idiopathic fetus with growth restriction (IFGR) and its relationship with the pathogenesis of IFGR. Methods In situ hybridization was used to detect the expression of HLA G mRNA and placental tissue in 20 cases of IFGR and 28 cases of normal maternal (control group). The placental tissues of both groups were observed for pathology. Results (1) The incidence of placental pathological changes in IFGR group was 75% (15/20), mainly chronic chorioamnionitis, placental infarction and villous growth retardation; it was significantly higher than 18% (5/28) in control group , The difference between the two groups was statistically significant (P = 0 001). (2) The positive expression rate of HLA G mRNA in placenta of IFGR group was 45% (9/20), which was significantly lower than 79% (22/28) in control group. The difference between the two groups was statistically significant (P = 0 017). (3) The positive expression of HLA G mRNA mainly located in the cytoplasm of placental villous extracytosynovial cells and syncytiotrophoblasts, showing a purple-blue granular precipitate with a clear outline. (4) There was a significant increase in the number of pathological changes of placenta compared with those with negative HLA G mRNA (r = -0 638, P = 00 008). Conclusion The expression of HLA GmRNA in placenta of IFGR patients decreased significantly. Abnormal expression of HLA G mRNA may be involved in the pathogenesis of IFGR.