中文摘要：

瞄准：由 transfecting artificial microRNA (amiRNA ) 调查肝炎 B (HBV ) 复制和表示的禁止的效果进 HepG2.2.15 房间。方法：三个 amiRNA-HBV 原生质标志被构造并且 transfected 进 HepG2.2.15 房间。HBV 抗原分泌物被解决时间的 fluoroimmunoassays (TRFIA ) 与短暂、稳定的 transfection 在房间检测。HBV DNA 复制被荧光检验 HBV S mRNA 的量的 PCR，和水平被半量的 RT-PCR 测量。结果：进 2.2.15 个房间的向量的短暂 transfection 的效率是 55%-60% 。所有向量在 transfection 以后在 72 h 和 96 h 在 HBsAg 和 HBeAg 上有重要抑制效果(P 【 0.01 为所有) 。进上层清液的 HBsAg 和 HBeAg 的分泌物被 49.8%+/- 禁止分别地， 6.7% 在在 amiRNA-HBV-S608 原生质标志 transfection 的 72 h 组织的 4.7% 和 39.9%+/- 。在文化上层清液以内的 HBV DNA 的拷贝显著地也在 transfection 以后在 72 h 和 96 h 被减少(P 【 0.01 为所有) 。在有稳定的 transfection 的房间，进上层清液的 HBsAg 和 HBeAg 的分泌物显著地在所有三个 transfection 组(0.01 为所有，对 negative 控制的 P 【 ) 被禁止。HBV DNA 的拷贝被 33.4%+/- 禁止 3.0% ， 60.8%+/-2.3% 和 70.1%+/-3.3% 分别地。结论：在 HepG2.2.15 房间， HBV 复制和表示能被指向编码区域的 HBV S 的人工的 microRNA 禁止。基于向量的人工的 microRNA 能是为长期的 HBV 感染的一条有希望的治疗学的途径。

英文摘要：

AIM： To investigate the inhibitory effects of hepatitis B virus （HBV） replication and expression by transfecting artificial microRNA （amiRNA） into HepG2.2.15 cells. METHODS： Three amiRNA-HBV plasmids were constructed and transfected into HepG2.2.15 cells. HBV antigen secretion was detected in the cells with transient and stable transfection by time-resolved fluoroimmunoassays （TRFIA）. HBV DNA replication was examined by ？ uorescence quantitative PCR, and the level of HBV S mRNA was measured by semi- quantitative RT-PCR. RESULTS： The efficiency of transient transfection of the vectors into 2.2.15 cells was 55%-60%. All the vectors had significant inhibition effects on HBsAg and HBeAg at 72 h and 96 h after transfection （P 〈 0.01 for all）. The secretion of HBsAg and HBeAg into the supernatant was inhibited by 49.8% ± 4.7% and 39.9% ± 6.7%, respectively, at 72 h in amiRNA- HBV-S608 plasmid transfection group. The copy of HBV DNA within culture supernatant was also significantly decreased at 72 h and 96 h after transfection （P 〈0.01 for all）. In the cells with stable transfection, the secretion of HBsAg and HBeAg into the supernatant was significantly inhibited in all three transfection groups （P 〈 0.01 for all, vs negative control）. The copies of HBV DNA were inhibited by 33.4% ± 3.0%, 60.8% ± 2.3% and 70.1% ± 3.3%, respectively. CONCLUSION： In HepG2.2.15 cells, HBV replication and expression could be inhibited by artif icial microRNA targeting the HBV S coding region. Vector-based artificial microRNA could be a promising therapeutic approach for chronic HBV infection.