摘要
目的 研究人巨细胞病毒 (humancytomegalovirus ,HCMV)感染人胚肺成纤维细胞 (humanembryoniclung ,HEL)后粘附分子 - 1(ICAM - 1)在基因转录水平的表达 ,探讨HCMV感染的发病机制。方法 采用RT -PCR技术研究细胞ICAM - 1- 1在基因转录水平的表达。结果 感染巨细胞病毒后ICAM - 1的表达上调 ,而UV灭活的CMV不能诱导I CAM - 1的上调 ,中药金叶败毒制剂与更昔洛韦 (Ganciclovir,GCV)不能阻止病毒诱导的ICAM - 1的上调 ,MEK特异性抑制子PD980 5 9可加强ICAM - 1的上调作用。结论 细胞ICAM - 1- 1在转录水平的上调可能是感染病毒的直接作用 ,MEK特异性抑制子PD980 5 9加强ICAM - 1上调作用。
Objective: To study the expression of intercellular adhesion molecule-1 in UV-inactivated virus, human Cytomegalovirus, and PD98059 and Jinyebaidu on human cytomegalovirus-infected fibroblasts, to determine the molecular mechanism of intercellular adhesion molecule-1 gene expression. Methods:The expression of ICAM-1 in human cytomegalovirus-infected fibroblasts and uninfected were evaluated by RT-PCR. Results: Our results indicate that intercellular adhesion molecule-1 expression was increased in human cytomegalovirus-infected fibroblasts compared with uninfected fibroblasts; Jinyebaidu did not suppress human cytomegalovirus induced upregulation of intercellular adhesion molecule-1 just like GCV. Interestingly, PD98059, a specific inhibitor of MEK enhanced HCMV-induced upregulation of ICAM-1 to some extent. Conclusion: The results suggest that upregulation of intercellular adhesion molecule-1 is the direct virus effect. PD98059 enhanced the upregulation of intercellular adhesion molecule-1.
出处
《中国优生与遗传杂志》
2004年第2期11-12,10,共3页
Chinese Journal of Birth Health & Heredity
基金
湖北省自然科学基金资助 (No .2 0 0 2AB13 2 )
