补肾活血周期治疗对宫腔粘连患者血清及子宫内膜TIMP-1表达的影响

Effects of Tonifying Kidney and Activating Blood Circulation Cycle Therapy on Expression of TIMP-1 in Serum and Endometrium of Patients with Intrauterine Adhesion

目的:通过观察宫颈粘连患者治疗前后血清及子宫内膜中基质金属蛋白酶抑制因子-1(tissue inhibitor of metalloproteinase-1,TIMP-1)的变化,探讨中药补肾活血周期治疗在宫腔镜术后再粘连预防中的作用机制。方法:100例宫腔粘连患者,按随机单盲法分为中药组(50例)和对照组(50例),2组均行宫腔镜下宫腔粘连分解术(transcervical resection of adhensions,TCRA)。术后中药组用中药补肾活血周期联合西药人工周期治疗,对照组单纯用西药人工周期治疗,用药3个月,再次进行宫腔镜检查。采用ELISA法和免疫组织化学S-P法检测治疗前后血清及子宫内膜中TIMP-1的表达。结果:治疗后2组患者粘连评分均下降(P<0.05),2组比较,差异有统计学意义(P<0.05);治疗后2组血清及子宫内膜中TIMP-1表达均降低(P<0.05),2组比较,差异均有统计学意义(P<0.05)。结论:中药补肾活血周期治疗能有效预防宫腔粘连术后再粘连,其机制与抑制TIMP-1的过度表达有关。

Objective： To observe the changes of TIMP- 1 in serum and endometrium of patients with intrauterine adhesion before and after treatment,and to explore the mechanism of Tonifying Kidney and Activating Blood Circulation cycle therapy on prevention of re-adhesion after hysteroscopic adhesiolysis. Methods： 100 patients with intrauterine adhesion were randomly divided into two groups with single blind,50 cases of each group. Both groups were performed TCRA. After operation,Tonifying Kidney and Activating Blood Circulation cycle therapy combined with artificial cycle therapy was given to the observation group and the control group received only artificial cycle therapy. The re- examination was performed after 3 months. The expression of TIMP-1 in serum and endometrium were detected by ELISA and immunohistochemical S- P assay. Results： After treatment,the adhesion score in both groups decreased and showed a significant difference（ P〈0. 05）,there was a significant difference between the two groups（ P〈0. 05）. After treatment,the expression of TIMP- 1 in serum and endometrium of both groups decreased and showed a significant difference（ P〈0. 05）,there was a significant difference between the two groups（ P〈0. 05）. Conclusion： Tonifying Kidney and Activating Blood Circulation cycle therapy could effectively prevent re-adhesion after hysteroscopic adhesiolysis,which the mechanism might be related to the inhibition of excessive expression of TIMP- 1.