bcl-2在腭裂胎鼠中间嵴上皮细胞的表达及意义  

Expression of bcl-2 in medial edge epithelial cells of cleft palate mice

作　　者：刘杨[1] 王浩宇[2] 安峰[3] 吴靖芳[2] 任君旭[2] 李瑞平[3] 

机构地区：[1]河北北方学院 [2]河北北方学院组胚教研室 [3]河北北方学院附属第一医院口腔科

出　　处：《北京口腔医学》2009年第3期143-145,共3页Beijing Journal of Stomatology

基　　金：河北省2006年医学科学研究重点课题计划项目(06238);张家口市科学技术研究与发展计划项目(061156)

摘　　要：目的研究地塞米松诱导的腭裂模型中腭突中间嵴上皮细胞(MEE)的变化及bcl-2基因表达,探讨MEE细胞凋亡与腭裂的关系。方法孕鼠随机分为实验组和对照组。实验组在11.5孕期日腹腔注射地塞米松,对照组注射等量生理盐水。分别于12.5、13.5、14.5、15.5、16.5孕期日(GD)处死,胎头石蜡包埋,切片,行HE和免疫组化染色。结果MEE细胞的形态变化:实验组和对照组12.5、13.5GDMEE细胞均为复层上皮,基底层细胞为立方形,表层覆以扁平细胞。对照组14.5GDMEE细胞在中线融合消失,实验组14.5～16.5GDMEE细胞继续生长变为多层,形成腭裂。免疫组化显示:12.5,13.5GD实验组和对照组MEE细胞的bcl-2表达无明显差别;实验组14.5GDMEE细胞bcl-2阳性信号明显强于对照组;15.5、16.5GD的阳性信号继续增强,而对照组MEE细胞消失。结论地塞米松可以通过影响bcl-2基因的表达,抑制MEE细胞凋亡,最终导致腭裂。Objective To examine the expression of bcl-2 in medial edge epithelial （MEE） cells and to investigate the relationship between the apoptosis of medial edge epithelialcells and cleft palate induced by dexamethasone （DEX）. Methods The pregnant mice were divided into experimental groups （EG） and control groups （CG） randomly. Dexamethasone and saline solution were then injected into the experimental group and controls at 11.5 GD respectively. The mice were killed by cervical dislocation at 12. 5,13.5,14. 5,15.5,16. 5GD. The embryonic heads were embeded,sectioned and stained by HE and bcl-2 immunohistochemistry. Results The MEE ceils of both groups had stratified epithelium on 12.5, 13.5GD. In control group the MEE cells fused and disappeared on 14.5GD, but in experimental group the MEE cells from 14. 5 - 16. 5 GD continued to grow and change to muhilayer,then developed cleft palate. There was no difference in bcl-2 expression between the two groups on 12. 5GD and 13. 5GD,but on ld. 5GD the staining was more intense in experimental group than in controls. Conclusion Dexamethasone could lead to cleft palate by influencing the expression of bcl-2 gene and inhibting apoptosis of MEE cells.

关 键 词：地塞米松 胎鼠 腭裂 BCL-2基因 

分 类 号：R78[医药卫生—口腔医学]