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140只 A 系小鼠在妊娠12~(14)时平分为实验组(注射20mg/kg地塞米松磷酸钠,DEX)和对照组(注射20mg/kg无菌蒸馏水),在妊娠第13~(14),13~(20),14~8,14~(14),14~(20),15~8,15~(20)7个不同时期处死小鼠,剖腹取胎,鼠头颅冠状连续切片观察鼠腭胚突发育形态变化。结果表明:DEX 诱发 A 系小鼠腭裂可导致使其腭突上提运动延迟12～14小时;A 系小鼠腭裂,主要是腭侧突未能在中线发生接触所致;DEX作用后 A 系小鼠颅面结构有过早骨化活动,可能和腭裂形成有关;DEX 作用 A 系小鼠后,腭突细胞受抑制,胞外基质形成不足,与腭突发育不足有关。
A group of 140 A mice were equally divided into experimental group (20mg / kg dexamethasone sodium phosphate, DEX injection) and control group (20mg / kg sterilized distilled water injection) at 12th to 14th gestation, Mice were sacrificed in 7 different periods of 14, 13, 20, 14, 8, 14, 14, 14, 20, 15, Changes in morphology of mouse palatal embryos were observed by sectioning. The results showed that: DEX induced cleft palate cleft palate in A-line mice resulted in 12- to 14-hour delay in cleft palate movement; cleft palate in A-line mice was mainly due to the palatal protuberance failed to contact in the midline; The craniofacial structure of mice had premature ossification activity, which may be related to the formation of cleft palate. After DEX treatment, the palatal cells were inhibited and the formation of extracellular matrix was insufficient, which was related to the underdevelopment of palatal palatal.