[Expression of PROK 1 and its receptor PROKR 1 in endometriosis and its clinical significance].

To investigate the role of prokineticin (PROK) 1 and prokineticin-receptor (PROKR) 1 in the pathogenesis of endometriosis and its clinical signifaicance. Methods: Quantitative real-time PCR (qPCR) and Western bloting were used to detect the expression of PROK 1 and PROKR 1 in eutopic and ectopic endometrium of endometriosis (n=22) and normal control endometrium (n=18). Endometrial stromal cells were isolated and cultured in 6 normal controls. The expression of PROK 1 mRNA was detected by qPCR after treated with estradiol (E2) or TNF-α. Results: PROK 1 and PROKR 1 mRNA were expressed in eutopic and ectopic endometrium of endometriosis and normal control endometrium, and the expression level gradually declined (P<0.05). The expression of PROKR-1 protein in eutopic and ectopic endometrium of endometriosis and normal control endometrium gradually declined (P<0.05). The expression of PROK-1 protein in normal control endometrial cells and eutopic endometrium cell was higher in secretory phase than in proliferative phase (P<0. 05). E2 did not change the expression of PROK 1, whereas TNF-α up-regulated the expression of PROK 1. Conclusion: PROK-1 and its receptors are involved in the pathogenesis and development of endometriosis. TNF-α can promote angiogenesis via up-regulating the expression of PROK 1.目的：探讨前动力蛋白-1(prokineticin 1，PROK 1)及其受体(prokineticin-receptor 1，PROKR 1)在子宫内膜异位症中的表达水平及意义。方法：采用定量PCR(quantitative PCR，qPCR)和蛋白质印迹法检测PROK 1和PROKR 1在18例正常对照组和22例子宫内膜异位症患者在位内膜及异位内膜中的表达水平；将6例正常对照组子宫内膜间质细胞分离、培养，给予雌二醇(estradiol，E2)及肿瘤坏死因子-α(tumor necrosis factor-α，TNF-α)干预后，采用qPCR检测PROK 1 mRNA的表达水平。结果：PROK 1 和PROKR 1 mRNA在子宫内膜异位症患者的异位内膜和在位内膜以及正常对照组子宫内膜中均有表达，表达最高的为异位内膜组，表达最低的为正常内膜组(P<0.05)；PROK 1 和PROKR 1 蛋白在子宫内膜异位症患者的异位内膜和在位内膜以及正常对照组的子宫内膜中均有表达，在异位内膜中表达最高，在正常内膜中表达最低(均P<0.05)；在正常子宫内膜组及子宫内膜异位症组中PROK 1的蛋白表达水平均为分泌期高于增生期(均P<0.05)；E2对子宫内膜间质细胞PROK 1 mRNA的表达无明显影响，TNF-α能上调子宫内膜间质细胞PROK 1 mRNA的表达。结论：PROK 1及其受体参与了子宫内膜异位症的发生并对其发展有促进作用，TNF-α可能上调PROK 1的表达从而促进血管生成。.