摘要
背景与目的:研究全反式视黄酸(All-TransRetinoicAcid,RA)对小鼠胚胎腮弓的致畸作用及其可能的致畸机制。材料与方法:采用植入后全胚胎培养观察RA对孕8.5d小鼠腮弓的致畸作用;采用5-溴脱氧尿嘧啶核苷(Bromodeoxyuridine,BrdU)标记及检测,切口末端标记法,切片和整体免疫组化观察RA对颅神经嵴细胞(Cranialneuralcrestcells,NCC)增殖、凋亡和迁移的影响。结果:RA诱导腮弓出现发育不良,发育不全,第一、二腮弓融合畸形;RA处理组腮弓BrdU掺入率减少,凋亡增加,NCC出现异常的迁移路径和方式。结论:RA诱导腮弓畸形,NCC增殖减少,凋亡增加,迁移改变是其可能的致畸机制。
BACKGROUND ＆ AIM ：To investigate the branchial arch malformations in all-trans retinoic acid （RA）-treated mouse embryos and its possible pathogenic pathways.MATERIAL AND METHODS：After whole embryo culture （WEC）, mouse embryos treated with RA were examined for dysmorphogenesis （Scanning Electron Microscopy）, cell proliferation （BrdU incorporation and detection method）, cell apoptosis （TUNEL method）, cranial neural crest cells （NCC） migration （sections and whole-mounts imInunohistochemistry） .RESULTS：During the whole culture period,RA-treated embryos showed branchial arch abnormalities including hypoplasia,agenesis, and fusion of first and second branchial arches. Increased apoptotic cells, decreased cell proliferation and anomalous NCC migration pathways were found in RA-treated embryos. CONCLUSION： These results suggested that branchial arches malformations induced by RA were related with the following possible pathogenetic mechanisms： increased cell apoptosis, inhibition of cell proliferation, and alteration of NCC migration.
出处
《癌变·畸变·突变》
CAS
CSCD
2006年第3期194-197,共4页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家"973"项目(No.2001CB510305)
国家自然科学基金(No.30371224)
北京市自然科学基金(No.7052040)
关键词
全反式视黄酸
腮弓畸形
神经嵴细胞
增殖
凋亡
迁移
all-trans retinoic acid
branchial arch malformations
neural crest cell
proliferation
apoptosis
migration pattern
