中文摘要：

瞄准：在肝炎 B (HBV ) 倡导者上探索核甙类似物 beta-L-D4A 和 beta-LPA 的效果。方法：四个 HBV 倡导者被聚合酶链反应(PCR ) 和克隆进表示向量 pEGFP-1 的潜水艇放大。HBV 倡导者控制的四 recombinants 被限制分析证实并且定序。有 recombinant 原生质标志的人的肝细胞瘤 HepG2 房间 transfected 与 beta-L-D4A 和 beta-LPA 的各种各样的集中被对待。然后，提高了绿荧光灯的蛋白质(EGFP ) 积极房间被萤光显微镜检查并且用荧光检测激活的房间 sorter (FACS ) 。结果：四个 HBV 倡导者独立被获得并且成功地克隆进 pEGFP-1。在表面倡导者(Sp ) 和 X 倡导者(Xp ) 的控制下面的 EGFP 的表示被 beta-L-D4A 以一种剂量依赖者方式禁止，当在核心倡导者(Cp ) 和 Xp 的控制下面的 EGFP 的表示被 beta-LPA 以一种剂量依赖者方式禁止时。结论：这里调查的二新奇核甙类似物能以一种剂量依赖者方式禁止 HBV 倡导者的活动。这些调查结果可以解释这二新奇混合物由禁止 HBV DNA 复制的行动的机制。

英文摘要：

AIM： To explore the effects of the nucleoside analogues β-L-D4A and β-LPA on hepatitis B virus （HBV） promoters. METHODS： Four HBV promoters were amplified by polymerase chain reaction （PCR） and subcloned into the expression vector pEGFP-1. The four recombinants controlled by HBV promoters were confirmed by restriction analysis and sequencing. Human hepatoma HepG2 cells transfected with the recombinant plasmids were treated with various concentrations of β-L-D4A and β-LPA. Then, enhanced green fluorescent protein （EGFP）-positive cells were detected by fluorescence microscopy and using a fluorescence activated cell sorter RESULTS： Four HBV promoters were separately obtained and successfully cloned into pEGFP-1, Expression of EGFP under the control of the surface promoter （Sp） and the X promoter （Xp） was inhibited by β-L-D4A in a dosedependent manner, while expression of EGFP under the control of the core promoter （Cp） and Xp was inhibited by β-LPA in a dose-dependent manner. CONCLUSION： The two novel nucleoside analogues investigated here can inhibit the activities of HBV promoters in a dose-dependent manner. These findings may explain the mechanisms of action by which these two novel compounds inhibit HBV DNA replication.