摘要
目的研究丙型肝炎病毒核心蛋白（HCV—core）在肝源性细胞系中与载脂蛋白AI（apoAI）的相互作用，为丙型肝炎病毒引起的脂肪肝的分子机制提供理论基础。方法构建真核表达质粒pcDNA3．1（-）-myc—his—apoAI、pcDNA3．1（-）-cole、pACT—apoAI和pBIND-core，共转染到HepG2细胞中。用免疫共沉淀（CoIP）和哺乳动物双杂交的方法检测HCV．cole与apoAI相互作用的关系，Westernblot方法分析免疫共沉淀杂交带，用DualLuciferase ReporterAssaySystem检测荧光素酶强度。结果CoIP试验显示有共沉带的出现，且大小正确。转染pACT—apoAI和pBIND—core组，相对荧光素酶活性值较pACT和pBIND空载体组明显升高。结论HCV．core可与apoAI在体内相互作用，为慢性丙型肝炎致肝脂肪变的机制研究提供理论依据。
Objective To study interaction of HCV core protein and apoA Ⅰ , and investigate the mechanism of this protein in fatty liver. Methods Constructed plasmid pcDNA3.1 （-）-myc-his-apoA I , pcDNA3.1 （-）-core, pACT-apoA I and pBIND-core, and co-transfered into HepG2 cells. The interaction of HCV core protein and apoA I was detected using the methods of co-immunoprecipitation （CoIP） and mam- malian two-hybrid system. Results ColP in vivo was assayed by Western blot and the immunoprecipitation appeared. The luciferase level in group pACT-apoAⅠ and pBIND-core was higher than that in the negative control. Conclusion HCV core protein and apoAⅠ can interact in vivo. This study provides new theory for the mechanism of chronicity hepatitis C in fatty liver.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2009年第8期697-700,共4页
Chinese Journal of Microbiology and Immunology
基金
基金项目：国家自然科学基金资助项目（10001105-4938-17）
