中文摘要：

目的探讨野生型和突变型CD59分子的表达与细胞凋亡因子之间的关系。方法应用免疫组化方法，分别测定空pIRES、野生型pIRES-WTCD59和突变型pIRES-MCD59转染CHO细胞中凋亡相关基因Caspase-3、Bcl-2的表达。结果转染野生型pIRES-WTCD59组与转染空pIRES质粒组比较，Caspase～3表达降低，Bcl-2表达增高，差异有显著性（Z=3．462、3．958，P〈0．05）；转染突变型pIRES-MCD59组与转染空pIRES质粒组比较，Caspase3表达降低，Bcl-2表达增高，差异有显著性（Z=3．212、3．956，P〈0．05）；转染野生型pIRES-WTCD59组与突变型pIRES-MCD59组比较，Caspase-3、Bcl-2表达差异无显著性（Z=1．948、0．544；P〉0．05）。结论CD59分子具有抑制凋亡的作用，而其保守位点W40与凋亡信号的传导无关。

英文摘要：

Objective To explore the relationship between wild-type and mutant CD59 and apoptotic factors. Methods Caspase-3 and Bcl-2 were detected by immunohistochemistry technique on empty pIRES, wild-type pIRES-WTCD59 and mutant pIRES-MCD59 transfected CHO cells. Results Compared with pIRES group, expression of Caspase-3 decreased （Z=3. 462, P〈0.05） and Bcl-2 increased （Z=3. 958,P〈0.05） in wild-type CD59 group, and Caspase-3 decreased （Z=3. 212 ,P（0.05） and Bcl-2 increased （Z=3. 956,P〈0.05） in mutant CD59 group. But there was no significant differences between wild-type and mutant groups in terms of Caspase-3 and Bcl-2 expressions （Z=1. 948,0. 544;P〈0.05）. Conclusion CD59 may have an effect on inhibiting apoptosis, and its conserved W40 site has no connection with the conduction of apoptotic signal.