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目的:研究CD59特异位点的短肽封条对HeLa细胞凋亡相关基因(survivin、caspase-3及bax)的表达作用,探讨CD59特异位点的短肽封条促HeLa细胞凋亡的作用机制。方法:将CD59特异位点的短肽封条分别作用于HeLa细胞和转CD59基因的HeLa细胞。作用24 h后,采用MTT的方法来检测细胞增殖抑制率;并利用免疫组织化学方法检测sur-vivin,caspase-3及其bax的表达水平。结果:转CD59基因的HeLa细胞+短肽的细胞组增殖抑制率大于HeLa细胞+短肽组(P<0.01)。转CD59基因的HeLa细胞+短肽组和正常的HeLa细胞+短肽组相比较,survivin表达水平降低(P<0.05);而caspase-3表达水平增高(P<0.05);bax的表达量各组比较,差别无统计学意义。结论:CD59特异位点的短肽封条具有下调survivin的表达,活化caspase-3,从而促进HeLa细胞的凋亡。
AIM: To investigate the expression of survivin, caspase-3 and bax in HeLa cells treated with short peptide fragments of CD59 specific locus, and to explore the mechanism of HeLa cell apoptosis induced by short peptide binding of CD59. Methods: HepG2 cells were transfected with HeLa cells and HeLa cells transfected with CD59 by using the short peptide seal of CD59. After 24 h treatment, MTT assay was used to detect the inhibition rate of cell proliferation. The expression of sur-vivin, caspase-3 and bax were detected by immunohistochemistry. Results: The proliferation inhibition rate of HeLa cells + short peptide transfected with CD59 gene was higher than that of HeLa + short peptide group (P <0.01). The expression of survivin in HeLa + short peptide group transfected with CD59 gene was significantly lower than that in normal HeLa + short peptide group (P <0.05), while the expression of caspase-3 was increased (P <0.05) Group comparison, the difference was not statistically significant. CONCLUSION: The short peptide of CD59 specific site can down-regulate the expression of survivin, activate caspase-3 and promote the apoptosis of HeLa cells.