层粘连蛋白和纤维粘连蛋白在过量维生素A酸致心脏畸形中的作用:免疫组织化学研究

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维生素A酸是常见的一类化学致畸因子,可引起各种心脏畸形,如主动脉骑跨、室间隔缺损等.实验采用免疫组织化学方法观察层粘连蛋白和纤维粘连蛋白在心脏正常和异常发育过程中的分布和变化规律,以探讨过量维生素A酸致心脏畸形发生的机理.结果显示:心内膜垫形成之前,心内膜细胞基底面呈层粘连蛋白和纤维粘连蛋白阳性;当内膜细胞转化为内膜垫细胞时,其基底面的层粘连蛋白和纤维粘连蛋白消失,心胶质和心肌膜中层粘连蛋白、纤维粘连蛋白免疫组化染色明显增强;心内膜垫形成并融合后,其染色又明显减弱.给孕鼠灌服过量的维生素A酸18小时后,各时间组胚胎心脏的心内膜、心胶质、心肌膜的层粘连蛋白和纤维粘连蛋白均出现了不同程度的减弱.这说明层粘连蛋白和纤维粘连蛋白是内膜垫细胞粘着和迁移的主要介导物质,维生素A酸抑制其两者的合成是引起心脏畸形的一个重要途径. Vitamin A acid is a common class of chemical teratogenic factors, can cause a variety of cardiac malformations, such as aortic riding, ventricular septal defect, etc. The experimental immunohistochemical staining laminin and fibronectin in the normal and abnormal heart In order to investigate the mechanism of heart deformity caused by excess vitamin A. The results showed that before the formation of endocardial cushion, the basal plane of endocardial cells was positive for laminin and fibronectin; when Membrane cells transformed into endometrial cells, the basal laminin and fibronectin disappeared, cardiac glia and myocardial membrane laminin, fibronectin immunohistochemical staining was significantly enhanced; endocardial cushion formation and fusion , And its staining was significantly weakened.Gastric acid in pregnant rats fed with excessive 18 hours later, the embryos at each time group of embryonic heart endocardium, cardiac glia, laminin and myocardial fibronectin appear different This suggests that laminin and fibronectin are the main mediators of adhesion and migration of endomembrane cells, and vitamin A inhibits the synthesis of both From heart malformations an important way.
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