摘要
目的研究生长激素释放激素拮抗剂对异位子宫内膜细胞增殖的作用及与cAMP信号通路的关系。方法异位子宫内膜组织采自子宫内膜异位症的妇女,分离异位子宫内膜基质细胞(ESC)。并加入GHRH拮抗剂JV-1-36培养。GHRH,GHRH受体(GHRH-R)和GHRH-R剪接变异体(SV)1 mRNA由反转录聚合酶链反应(RT-PCR)检测,细胞增殖通过细胞对BrdU的摄入来检测,放免法检测细胞内cAMP水平。结果 GHRH-R mRNA表达于ESC,而不表达于正常子宫内膜组织;SV1mRNA表达于正常子宫内膜及ESC。GHRH拮抗剂JV-1-36能降低异位子宫内膜基质细胞cAMP,减少细胞BrdU摄入。结论GHRH拮抗剂JV-1-36能抑制异位子宫内膜基质细胞增殖,其机制可能与cAMP信号通路有关。
Objective To study the inhibitory effect of GHRH antagonists on ectopic endometrial cell proliferation may be act through cAMP signal pathway. Methods Ectopic endometrial tissues were collected from women with endometriosis. Human eetopic en- dometrial stromal cells(ESC) were isolated and cultured. ESC were treated with GHRH antagonist JV - 1 -36. Expression of GHRH, GHRH receptor (GHRH -R) and GHRH -R splice variant (SV)1 mRNA were determined by reverse -transcription polymerase chain reaction ( RT - PCR). The ESC proliferation was assessed by 5 - bromo - 2 - deoxyuridine incorporation. Cyclic adenosine monophosphate (cAMP) levels was studied by ELISA. Results The ESCs,but not normal endometrial tissues, expressed GHRH - R mRNA. SV1 mR- NA was determined in normal endometrial tissues. In ESCs,JV -1 -36 reduced cAMP production and incorporation of BrdU. Conclusion GHRH antagonist JV - 1 - 36 can inhibit the proliferation of ectopic endometrial stromal cells and its mechanism may be related to the cAMP signaling pathway.
出处
《医学研究杂志》
2013年第5期103-106,共4页
Journal of Medical Research
基金
浙江省医药卫生科技研究计划项目(2009B145)