孕激素受体与TNF-α、IL-1β、NF-κB在自然流产蜕膜组织中的表达及临床意义

Expression and Clinical Significance of Progesterone Receptor,TNF-α,IL-1β and NF-κB in Decidua of Unexplained Recurrent SpOntaneousAbortion Patients

目的:探讨孕激素受体(Progesterone receptor,PR)与TNF-α、IL-1β、NF-κB在不明原因自然流产蜕膜组织中的表达及临床意义。方法:收集不明原因自然流产病例(研究组)和正常早孕人工流产病例(对照组)各33例。采用实时荧光定量PCR(qRT-PCR)法检测两组蜕膜组织中PR、TNF-α、IL-1β、NF-κB的表达差异,并分析TNF-α、IL-1β、NF-κB及PR间的相互关系。结果:与正常人工流产蜕膜组织比较,不明原因自然流产蜕膜组织PR mRNA表达明显降低(P=0.011),而NF-κB、TNF-α和IL-1βmRNA表达明显增强(P<0.001,P=0.008,P=0.009)。相关性分析显示,不明原因自然流产蜕膜组织中PR表达与NF-κB表达明显负相关(r=-0.508,P<0.013),而TNF-α和IL-1β的表达均与NF-κB的表达显著正相关(r=0.680,P<0.001,r=0.670,P<0.001)。结论:TNF-α、IL-1β及NF-κB表达增加和PR表达减少与不明原因自然流产有关,即PR的减少可能是导致不明原因自然流产的因素之一,可能与NF-κB的激活启动炎性反应有关。

Objective To study the expression and clinical significance of progesterone receptor（PR）,TNF-α ,IL-1β and NF- K B in uterine decidua of unexplained recurrent SpOntaneous abortion patients.Methods Real-time PCR（qRT-PCR） was used to detect the expression of PR,TNF-α ,IL-1β and NF- K B in the decidua of SpOntaneous abortion and normal pregnancy（33 cases in each group,respectively）,and the correlation among the PR,TNF-α ,IL-1βand NF-K B were analysed.Results Compared to file normal pregnancy（control group）,the mRNA expression of PR was significantly decreased（P=-0.011）,but the mRNA expression of TNF-α ,IL-1β and NF- K B was significantly increased in the decidua of unexplained recurrent SpOntaneous abortion（P 〈 0.001,P=0.008,P=0.009,respectively）.The correlation analysis showed that,in the decidua of unexplained recurrent SpOntaneous abortion,there was a negative correlation between the expression of PR and NF-K b（r= - 0.508,P 〈 0.013）,but the expression of TNF-α and ,IL-1βhad a positive correlation with NF-Kb（r=0.680,P 〈 0.001,r=0.670,P〈 0.001,respectively）. Conclusion High expression of TNF-α ,IL-1β and NF-Kb,and low expression of PR may be involved in the pathogenesis of unexplained recurrent SpOntaneous abortion.That is to say,the expression of PR down-regulated may be lead to SpOntaneous abortion,which may be correlated with the NF- K B abnormal activated and initiating the inflammation.