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目的通过检测胎儿生长受限(fetal growth restriction,FGR)患者胎盘、外周血中单核细胞趋化蛋白-1(monocyte chemoattractant protein-1,MCP-1)的表达水平,探讨MCP-1在FGR中的作用及可能机制。方法选择50例FGR患者为FGR组,正常晚期妊娠分娩孕妇50例为正常对照组,以酶联免疫吸附法检测两组孕妇胎盘、外周血MCP-1水平,并对胎盘组织切片进行病理形态学分析。结果 FGR组胎盘光镜下见不同程度的绒毛发育不良,合体结节增多,绒毛炎,其发生率高于正常对照组[64.0%(32/50)vs12.0%(6/50),P<0.05],其中合并绒毛炎的发生率31%(10/32);FGR组中胎盘病理异常组的胎盘MCP-1浓度高于正常对照组,差异有统计学意义[胎盘MCP-1:(136.97±10.24)vs(129.76±5.67)ng/m L,P<0.05],其中合并绒毛炎胎盘中MCP-1浓度高于正常对照组[(149.76±8.67)vs(129.76±5.67)ng/m L,P<0.05];而FGR组中胎盘病例异常组与正常对照组外周血MCP-1浓度比较差异无统计学意义[血清MCP-1(137.14±9.73)vs(140.16±10.34)ng/m L,P>0.05]。结论 MCP-1参与了FGR的发生,其作用机制可能通过过度炎症反应,导致胎盘灌注不足。
Objective To investigate the expression of monocyte chemoattractant protein-1 (MCP-1) in the placenta and peripheral blood of patients with fetal growth restriction (FGR) The role and possible mechanism. Methods Fifty FGR patients were selected as the FGR group. Fifty pregnant women with normal late pregnancy were selected as the normal control group. The levels of MCP-1 in the placenta and peripheral blood of the two groups were detected by enzyme-linked immunosorbent assay. The histopathology analysis. Results The placenta of FGR showed different degrees of villous dysplasia, increased nodules and villus inflammation, which were significantly higher than those in the control group [64.0% (32/50) vs 12.0% (6/50), P <0.05], and the incidence of villus inflammation was 31% (10/32). The placental MCP-1 concentration in placental dysplasia group in FGR group was higher than that in normal control group [the difference was statistically significant [placental MCP-1 :( (149.76 ± 8.67) vs (129.76 ± 5.67) ng / m (136.97 ± 10.24) vs (129.76 ± 5.67) ng / m L, P <0.05] L, P <0.05]. However, there was no significant difference in MCP-1 levels in the peripheral blood between the abnormal placenta group and the normal control group in FGR group [serum MCP-1 (137.14 ± 9.73) vs (140.16 ± 10.34) ng / m L, P> 0.05]. Conclusion MCP-1 is involved in the pathogenesis of FGR. Its mechanism may be due to excessive inflammation, resulting in insufficient placental perfusion.