妇炎康联合物理因子治疗慢性盆腔炎的疗效及对微小RNA-224-3P及转化生长因子β/Smad信号通路表达的影响

Efficacy of Fuyankang combined with physical agents therapy for chronic pelvic inflammatory disease and its effect on expression of microRNA-224-3p and transforming growth factor beta/Smad signaling pathway

目的探讨妇炎康联合物理因子治疗慢性盆腔炎(CPID)的疗效及对微小RNA(miRNA)-224-3P及转化生长因子β(TGF-β)/Smad信号通路表达的影响。方法将62例CPID患者随机分为观察组和对照组,每组31例。对照组给予诺氟沙星和甲硝唑抗感染治疗,观察组在对照组治疗方案基础上,给予妇炎康联合物理因子治疗。治疗1个疗程后,比较两组患者血清miRNA-224-3P、TGF-β1、Smad-3和Smad-7水平及治疗效果。结果治疗后,两组患者血清miRNA-224-3P、TGF-β1和Smad-3水平均较治疗前降低,Smad-7水平较治疗前升高,且观察组血清miRNA-224-3P、TGF-β1和Smad-3水平低于对照组,Smad-7水平高于对照组,观察组疗效优于对照组(均P<0.05)。结论妇炎康联合物理因子治疗CPID患者的疗效优于常规抗感染治疗,可能与其通过调节miRNA-224-3P和TGF-β/Smad信号通路表达从而抑制炎症反应有关。

Objective To investigate the efficacy of Fuyankang combined with physical agents therapy for chronic pelvic inflammatory disease(CPID)as well as its effect on the expression of microRNA(miRNA)-224-3p and transforming growth factor beta(TGF-β)/Smad signaling pathway.Methods Sixty-two CPID patients were randomly divided into observation group and control group,with 31 cases in each group.The control group received norfloxacin and metronidazole for anti-infection treatment,while the observation group received Fuyankang combined with physical agents therapy on the basis of the therapeutic regimen in the control group.After one course of treatment,serum levels of miRNA-224-3p,TGF-β1,Smad-3 and smad-7,and therapeutic effects were compared between the two groups.Results After treatment,serum levels of miRNA-224-3P,TGF-β1 and Smad-3 were lower and Smad-7 level was higher in the two groups in comparison with the levels before treatment,moreover,compared with the control group,the observation group had lower levels of serum miRNA-224-3P,TGF-β1 and Smad-3,higher Smad-7 level,and superior efficacy(all P<0.05).Conclusion Fuyankang combined with physical agents therapy has superior efficacy for CPID patients than routine anti-infection treatment,which may be related to the inhibition of inflammatory response by regulating the expression of miRNA-224-3p and TGF-β/Smad signaling pathway.