摘要
目的:通过比较正常妊娠模型小鼠及自然流产模型小鼠蜕膜细胞凋亡及Bcl-2、Bax蛋白的表达,从细胞及分子水平探讨自然流产的发病机制。方法:建立正常妊娠模型CBAXBALB/c和自然流产模型CBAXDBA/2。用免疫组化SABC法测定两组模型孕13天蜕膜细胞Bcl-2和Bax蛋白的表达,并通过MIAS-2000医用彩色病理图像免疫组化测量系统对其表达进行半定量分析,其结果用平均灰度值表示;同时应用DNA缺口原位末端标记技术(TUNEL)测定两组模型孕13天蜕膜细胞凋亡情况。结果:与正常妊娠模型相比,自然流产模型蜕膜细胞Bcl-2蛋白的表达降低(P<0.01);Bax蛋白的表达明显升高(P<0.01)。蜕膜细胞凋亡指数,自然流产模型明显高于正常妊娠模型(P<0.01)。结论:早孕期蜕膜组织细胞凋亡异常是自然流产的机制之一,Bcl-2/Bax途径可能是诱导早孕期蜕膜细胞凋亡的重要因素。
Objective:To study the pathological mechanism for spontaneous abortion by determining apoptosis and expression of Bcl-2 as well as Bax in decidua tissue of spontaneous abortion models and normal pregnancy mice.Methods: The abortion-prone CBAXDBA/2 matings were established as the model of spontaneous abortion and the nonabortion-prone CBAXBALB/c matings were used as the model of normal pregnancy. SABC was used to detect the expression of Bcl-2 and Bax in decidua tissue of spontaneous abortion and normal pregnancy at day 13 of gestation. Medical color-image measure system for immune-histochemistry was used for semiquantitative analysis. Apoptosis was detected by in situ TUNEL assay. Results: In decidua tissue of the spontaneous abortion models, Bcl-2 expression was lower and Bax was higher than it that of normal model (P 〈 0.01) ; resucting in significantly decreased Bcl-2/Bax ratio( P 〈 0.01). In spontaneous abortion model, apoptotic index (AI)of decidua tissue was significantly higher than in normal pregnancy( P 〈 0.01 ). Conclusion: Breaking the regulation of decidual tissue apoptosis may directly or indirectly results in spontaneous abortion during early gestation. The channel of Bcl-2/Bax systems may be one of the mechanisms for spontaneous abortion decidua apoptosis.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2008年第7期637-639,共3页
Chinese Journal of Immunology
基金
国家人口计生委资助项目([2005]11号(1-4))
大同市科技成果推广项目([2005]第61号-2-69)