摘要
目的考察丙型肝炎病毒核心蛋白对细胞凋亡的影响,以期从另一个角度研究丙型肝炎病毒可能的致癌机理.方法应用流式细胞仪检测 HepG2-C 细胞和 HepG2-CMV 细胞对氨甲喋呤(MTX 10mg/L)和去血清的耐受.并进一步检测凋亡相关基因及产物的表达.结果应用流式细胞仪检测 HepG2-C 细胞和 HepG2-CMV 细胞对氨甲喋呤(MTX 10mg/L)的耐受,结果 HepG2-C 细胞24小时和48小时的凋亡率分别为5.1%和9.6%,而 HepG2-CMV 细胞为6.8%和16%.而去血清2,4,6天的 HepG2-C 细胞凋亡率分别为6.6%,9.4%,11.5%,而 HepG2-CMV 细胞分别为11.4%、13.5%、16.1%.表明表达丙肝病毒核心蛋白的细胞 HepG2-C 较转染空载体的细胞 HepG2-CMV 耐受凋亡.在进一步分子机理的探讨中发现 HepG2-C 细胞 P53,C-myc,Bcl-2表达增加,而 Fas 表达减低,转录水平也发生同样的变化.结论丙肝病毒核心蛋白可能通过调节基因转录与表达,抑制某些因素引起的细胞凋亡.
AIM To evaluate the effect of HCV core protein on apoptosis in HepG2 cells and to clarify the hapatocarcinogenic mechanism for HCV. METHODS The HepG2-C and HepG2-CMV cells were cultured with MTX and cultured in 1640 medium without serum.The apoptosis was examined with FCM.The apoptotic rates of HepG2-C at 24h and 48h after MTX addition were 5.1% and 9.6% respectively,and those at 2nd,4th and 6th day after serum withdrawal were 6.6%, 9.4%,11.5% respectively.While those of HepG2-CMV cells were 6.8% and 16% respectively after MTX addition, and 11.4%,13.5% and 16.1% after serum withdrawal respectively.In the further study of molecular mechanism,it was found that expression of p53,C-myc and Bcl-2 were increased,while Fas was decreased,and the same changes happened in transcription. RESULTS It was shown that HCV C protein could inhibit hepatocyte apoptosis induced by some stimuli.In the further study of molecular mechanism,the expression and transcription of p53,C-myc and Bcl-2 were increased, while the fas was decreased. CONCLUSIONS HCV C protein can inhibit hepatocyte apoptosis by modulating gene transcription and expression.It suggest that HCV C protein may contribute to viral carcinogenesis.
出处
《世界华人消化杂志》
CAS
2001年第10期1125-1128,共4页
World Chinese Journal of Digestology
基金
国家自然科学基金资助课题.No.39900176.
