CAJ | 학술논문

背景与目的:探索建立发生率高、畸形类型明确且易于获得的化学物致小鼠胎鼠短肢畸形的模型的方法.材料与方法:ICR小鼠合笼后,查到阴栓当天为孕期第0天(IGD0),孕鼠共50只,随机分为GD9、GD10、GD11、GD12给全反式视黄酸(all-trans-retinoic acid,atRA)实验组和对照组,共5组,每组10只,实验组经口灌胃1次给予孕鼠80 mg/kg atRA,对照组则给予等体积的大豆油,于GD18将孕鼠处死并取出胎鼠,观察不同时间给予孕鼠atRA的胎鼠的短肢畸形情况.结果:于GD10给予孕鼠atRA,可致胎鼠双前肢短小,肱骨、桡骨、尺骨均较正常组短(P均<0.05);于GD11给予孕鼠atRA,可致胎鼠双前肢和双后肢短小.肱骨、桡骨、尺骨、股骨、胫骨均较正常组短(P均<0.05),腓骨常缺失;于GD12给予孕鼠atRA,可致胎鼠尺骨较正常组短(P<0.05). 结论:成功建立了全反式视黄酸致小鼠短肢畸形的模型,为进一步研究肢体畸形的分子机制奠定了基础.
배경여목적:탐색건립발생솔고、기형류형명학차역우획득적화학물치소서태서단지기형적모형적방법.재료여방법:ICR소서합롱후,사도음전당천위잉기제0천(IGD0),잉서공50지,수궤분위GD9、GD10、GD11、GD12급전반식시황산(all-trans-retinoic acid,atRA)실험조화대조조,공5조,매조10지,실험조경구관위1차급여잉서80 mg/kg atRA,대조조칙급여등체적적대두유,우GD18장잉서처사병취출태서,관찰불동시간급여잉서atRA적태서적단지기형정황.결과:우GD10급여잉서atRA,가치태서쌍전지단소,굉골、뇨골、척골균교정상조단(P균<0.05);우GD11급여잉서atRA,가치태서쌍전지화쌍후지단소.굉골、뇨골、척골、고골、경골균교정상조단(P균<0.05),비골상결실;우GD12급여잉서atRA,가치태서척골교정상조단(P<0.05). 결론:성공건립료전반식시황산치소서단지기형적모형,위진일보연구지체기형적분자궤제전정료기출.
BACKGROUND AND AIM: To develop a chemically-induced, easily established short limb malformation model with high incidence rate and discrete abnormal phenotype. MATERIALS AND METHODS: After the male and female ICR mice copulated, the presence of vaginal plug the following morning was considered as gestational day 0 (GDO) . At GD9, GD10, GD11 and GD12, the pregnant mice in the treatment group were treated with 80 mg/kg all-trans-retinoic acid (atRA) , and those of the control group received the same volume of soybean oil. At GD18, pregnant mice were killed and the embryos were harvested. The abnormalities of the embryos in the treatment group were studied. RESULTS: In the group pregnant mice were treated with atRA at GD10, the forelimbs of embryos were short and small, and the humerus, radius and ulna were shorter than those of the control group. In the group treated with atRA at GD11, the forelimbs and the hindlimbs of embryos were short and small, and the humerus, radius, ulna, femur and tibia were shorter than those of the control group, and most of the embryos had no fibula. In the group treated with atRA at GD12, the ulna of the embryos were shorter than those of the control group. CONLUSION: We developed a model of short limbs induced by atRA during ICR mouse embryogenesis, providing a basis to investigate the molecular mechanism of limb deformity.