摘要
目的 :通过观察米非司酮对子宫肌层异位内膜组织细胞凋亡的影响 ,探讨子宫腺肌病的发病机制。方法 :确诊后的 5 0例患者 ,分成两组 ,实验组 2 5例 ,用药前行卵功、肝肾功能检查 ,结果回报正常后 ,给予口服 RU4 86 2 5 mg/ d,每日一次 ,连服 2 w。另外 2 5例为对照组。 5 0例患者均选择在月经增生期 ,月经后 3～ 7d,实验组开始服药 ,停药后立即手术 ;对照组住院后立即手术 ,手术切除子宫 ,取少许子宫异位内膜组织蜡块包埋待检。切除的子宫全部送病理。将 5 0块包埋的蜡块经处理后 ,采用原位末端酶标记技术检测细胞凋亡数 ,计算出凋亡指数 ,免疫组化法检测抗凋亡基因 Bcl- 2及促凋亡基因 Fas的表达水平。结果 :服米非司酮的实验组细胞凋亡指数平均为 11%± 9% ,而对照组细胞凋亡指数平均为 0± 0 .4 % ,两组比较有显著差异 ,P<0 .0 1。RU4 86可以下调 Bcl- 2基因 ,使其在子宫腺肌病患者子宫肌层的内膜中表达减低 ,Fas基因表达增强。结论 :米非司酮使子宫肌层异位内膜组织细胞凋亡指数增加 ,Bcl- 2表达降低 ,Fas表达增强。从而证实 ,米非司酮可诱导异位内膜组织细胞凋亡 ,抑制异位细胞生长 ,控制子宫腺肌病的发展 。
Objective:To explore the pathogenesis of adenomyosis in studing the effect of mifepritone to apoptsis cells in the utrine myometrium ectopic enometrial tissue Methods:Fifty inpatients were studied, patiens,who were willing to require being oprated after diagnosis ,must be women of 30~50 ages with nomal menstrual period and have not taken hormones drug in the last 3 months,were divided to two groups 25 cases were taken RU 486 25 mg / day and continually took for 2 weeks as investigative group Other 25 cases haven't taken any drug as control group 50 patiens were in the proliferative phase their menstrual cycle Did ovary function?liver function and then function before taking drug Apaptosis cells were detected by TdT mediated bio dUTP nick endlabeling(TUNEL) method Bcl 2 gene and Fas antigen expression demonestrated by immunohistochemistry Results:The apoptosis index was increased in the ectopic endometrial cells 11±9% ascompared to ectopic endopmetrial cells in control grops 0± 0 4%( P <0 01) Bcl 2 gene expression were significantly lower than of control and Fas antigen expression higher than that of coutrol Conclusion:RU486 induced apoptosis in the uterine myometriumectopic endometrial tissue It controlled adenomyosis inhibit cells growth in ectopic endomrtrial It found a new way for non operation treatmenomyosis
出处
《中国妇幼保健》
CAS
2004年第1期37-39,共3页
Maternal and Child Health Care of China
