CAJ | 학술논문

为探讨 ROS在小鼠月经样模型中的作用，将雌性 C57小鼠去势，序惯性的给予雌二醇（E2）或孕酮（P4），模拟增殖期和分泌期，花生油注射至宫腔以人工诱导蜕膜化，将孕酮皮埋管移除以造成孕酮的撤退，建立小鼠月经样模型，并在孕酮撤退前1、3、7 h 给予抗氧化剂NAC消除ROS，利用大体变化、阴道细胞学涂片和组织形态学方法检测子宫的状态，并利用氮蓝四唑（NBT）染色的组织超氧阴离子色度法检测 ROS的含量，以研究 ROS 在月经发生过程中对子宫内膜崩解的作用。阴道细胞学涂片显示，350 mg／kg 和500 mg／kg NAC能够抑制子宫内膜的出血，而200 mg／kg NAC则不能，子宫大体和组织形态学结果显示，350 mg／kg 和500 mg／kg NAC能够抑制子宫内膜的崩解，而200 mg／kg NAC则不能，同时，350 mg／kg和500 mg／kg NAC能够显著抑制ROS的产生，而200 mg／kg NAC则没有。说明350 mg／kg是抑制子宫内膜崩解的合适剂量，且ROS对子宫内膜的崩解起至关重要的作用。
위탐토 ROS재소서월경양모형중적작용，장자성 C57소서거세，서관성적급여자이순（E2）혹잉동（P4），모의증식기화분비기，화생유주사지궁강이인공유도세막화，장잉동피매관이제이조성잉동적철퇴，건립소서월경양모형，병재잉동철퇴전1、3、7 h 급여항양화제NAC소제ROS，이용대체변화、음도세포학도편화조직형태학방법검측자궁적상태，병이용담람사서（NBT）염색적조직초양음리자색도법검측 ROS적함량，이연구 ROS 재월경발생과정중대자궁내막붕해적작용。음도세포학도편현시，350 mg／kg 화500 mg／kg NAC능구억제자궁내막적출혈，이200 mg／kg NAC칙불능，자궁대체화조직형태학결과현시，350 mg／kg 화500 mg／kg NAC능구억제자궁내막적붕해，이200 mg／kg NAC칙불능，동시，350 mg／kg화500 mg／kg NAC능구현저억제ROS적산생，이200 mg／kg NAC칙몰유。설명350 mg／kg시억제자궁내막붕해적합괄제량，차ROS대자궁내막적붕해기지관중요적작용。
To explore the function of ROS in mouse menstrual-like model,female C5 7 mice were ovariecto-mized,and treated with the hormone to mimic the proliferation and secretoty period.After oil was inj ected into uterus luminal,49 h later,P4 explant was removed to mimic the P4 withdrawal to build the mouse menstrual-like model.Different doses of NAC(200 mg/kg,350 mg/kg and 500 mg/kg)were administrated to mice at-1 h(P4 withdrawal was regarded as 0 h),3 h,7 h and 1 1 h to exclave the ROS.The uterus was assayed by vananial smear,morphogy and histomorphology method,the level of ROS in the uterus was measured by superoxide anion assay kit.ROS levels were significantly increased before endometrial break-down in a mouse menstrual-like model.Vaginal smear inspection,morphology of uterine horns,and endom-etrial histology examination showed that 350 mg/kg and 500 mg/kg NAC obviously inhibited the endome-trial breakdown and shedding,but 200 mg/kg did not in this model.ROS plays a key role in endometrial breakdown and shedding.