摘要
目的:研究重组真核载体PcDNA3.1-MxA体外抗HBV的作用,为研究MxA基因(myxovirus-resistant A)治疗慢性HBV感染奠定基础。方法:将构建成功的重组真核载体PcDNA3.1-MxA转染入HepG2.2.15。将HepG2.2.15分为实验组(转染PcDNA3.1-MxA的HepG2.2.15)和对照组(转染PcDNA3.1的HepG2.2.15),应用RT-PCR方法检测两组HepG2.2.15内MxA mRNA(P<0.01),并应用ELISA法检测两组HepG2.2.15内HBsAg、HBeAg的水平。结果:RT-PCR扩增结果显示实验组的MxA mRNA水平均较对照组明显升高,实验组HBsAg、HBeAg水平明显低于对照组(均P<0.01)。结论:转染重组真核载体PcDNA3.1-Mx AHepG2.2.15内MxA蛋白明显抑制了HBV DNA的复制及表达,为进一步研究MxA蛋白体内抗病毒作用提供理论。
Objective: To investigate the anti-HBV effects of the recombinant eukaryotic plasmid PcDNA3. 1-MxA in HepG 2.2.15 cells in vitro. Methods: The recombinant eukaryotic plasmid PcDNA3.1-MxA was transfected into HepG 2.2.15 cells with Lipofection after extracted and confirmed with restrictive endonuclease analysis. The control group was HepG2.2.15 cells transfected with PcDNA3.1. The levels of MxA mRNA were detected by RT-PCR and the titers of HBsAg and HBeAg in supernatant liquids were detected by ELISA. Results: The RT-PCR results showed the level of MxA mRNA in the treatment group was much higher than that in the control group. The titers of HBsAg and HBeAg in supernatant liquid of the treatment group were significantly lower than those in the control group cells(P〈0.01 ). Conclusion : The study indicates that MxA protein can inhibit replication and expression of HBV.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2010年第1期46-48,共3页
Journal of Chongqing Medical University