CAJ | 학술논문

目的:探讨三氧化二砷(arsenic trioxide, ATO)对人子宫内膜癌HEC-1-A细胞生长的抑制作用.方法:采用MTT法比较ATO、孕酮、安宫黄体酮(medroxyprogesterone acetate,MPA)和顺铂(cisplatin, CDDP)对HEC-1-A细胞的抑制作用,应用FCM和DNA电泳检测ATO对细胞周期和细胞凋亡的影响.建立裸鼠人子宫内膜癌移植瘤动物模型,随机分为ATO低(4 mg·kg-1·d-1)、中(6 mg·kg-1·d-1)、高(8 mg·kg-1·d-1)剂量组、阳性对照CDDP组(3 mg·kg-1·d-1)及阴性对照组,腹腔连续给药14 d,计算肿瘤体积和肿瘤质量抑制率.结果:1～20 μmol/L ATO和CDDP可明显抑制细胞生长,且ATO 对细胞的抑制作用强于CDDP.5 μmol/L ATO作用后可导致细胞凋亡,并使细胞周期阻滞于S和G2/M期.低、中、高剂量ATO组和CDDP组的肿瘤体积抑制率分别为50.97%、75.58%、56.92%和52.23%,肿瘤质量抑制率分别为10.15%、29.33%、16.67%和14.69%,与阴性对照组相比差异有统计学意义(P＜0.05).结论:ATO可抑制HEC-1-A细胞及鼠荷人子宫内膜癌移植瘤的生长,有望成为治疗子宫内膜癌的新型药物.
목적:탐토삼양화이신(arsenic trioxide, ATO)대인자궁내막암HEC-1-A세포생장적억제작용.방법:채용MTT법비교ATO、잉동、안궁황체동(medroxyprogesterone acetate,MPA)화순박(cisplatin, CDDP)대HEC-1-A세포적억제작용,응용FCM화DNA전영검측ATO대세포주기화세포조망적영향.건립라서인자궁내막암이식류동물모형,수궤분위ATO저(4 mg·kg-1·d-1)、중(6 mg·kg-1·d-1)、고(8 mg·kg-1·d-1)제량조、양성대조CDDP조(3 mg·kg-1·d-1)급음성대조조,복강련속급약14 d,계산종류체적화종류질량억제솔.결과:1～20 μmol/L ATO화CDDP가명현억제세포생장,차ATO 대세포적억제작용강우CDDP.5 μmol/L ATO작용후가도치세포조망,병사세포주기조체우S화G2/M기.저、중、고제량ATO조화CDDP조적종류체적억제솔분별위50.97%、75.58%、56.92%화52.23%,종류질량억제솔분별위10.15%、29.33%、16.67%화14.69%,여음성대조조상비차이유통계학의의(P＜0.05).결론:ATO가억제HEC-1-A세포급서하인자궁내막암이식류적생장,유망성위치료자궁내막암적신형약물.
Objective:To explore the inhibitory effect of arsenic troixide (ATO) on the growth of human endometrial cancer HEC-1-A cells in vitro and in vivo. Methods:Tetrazolium salt assay (MTT) was used to compare the inhibitory effect of ATO on HEC-1-A cells with that of progesterone, medroxyprogesterone acetate (MPA) and cisplatin (CDDP). Flow cytometry and DNA electrophoresis were used to determine the effects of ATO on cell cycle and apoptosis. Human endometrial cancer xenografted model was established in nude mice. The tumor-bearing nude mice were randomly divided into the experimental groups: ATO low dose group (4 mg·kg-1·d-1), medium dose group (6 mg·kg-1·d-1), high dose group (8 mg·kg-1·d-1), CDDP positive control group (3 mg·kg-1·d-1) and saline negative control group. The drugs were administered intraperitoneally for 14 consecutive days, and then the tumor volume and tumor inhibition rate were calculated. Results: ATO 1-20 μmol/L and CDDP markedly inhibited the cell growth. The inhibitory effect of ATO was higher than that of CDDP. ATO 5 μmol/L treatment induced apoptosis and arrested cells at S and G2/M phase. ATO 4, 6, and 8 mg·kg-1·d-1 and CDDP 3 mg·kg-1·d-1 inhibited tumor volume by 50.97%, 75.58%, 56.92%, and 52.23%, respectively; and inhibited the tumor weight by 10.15%, 29.33%, 16.67%, and 14.69%, respectively. The difference was significant compared with negative control group (P<0.05). Conclusion:ATO inhibited the growth of endometrial cancer cells HEC-1-A in vitro and in vivo. It may become a novel therapeutic reagent for the treatment of endometrial cancer.