中文摘要：

人的 enterovirus (EV71 ) 71 是在亚洲的手，脚，和嘴疾病(HFMD ) 的最近的大规模爆发的主要原因的代理人。当前，没有为 HFMD 的预防和处理可得到的药。在这研究，我们比较了传统地为流行疾病的处理和预防被使用了的分别地，从中国植物汉语大黄， Artemisia carvifolia 和距骨提取的三自然混合物，感冒 emodin， artemisinin 和 astragaloside 的 anti-EV71 活动。人的肺成纤维细胞房间线 MRC5 与 EV71 感染嘲笑或感染，并且与药对待。这些药的 cytotoxicity 与 MTT 试金被检测。象房间死亡和压缩原子核那样的 cytopathic 效果词法上被观察。为 EV71 染色体复制要求的编码 VP1 顺序是有 qRT-PCR 的 assayed。病毒的蛋白质表示与西方的弄污被分析。病毒的 TCID50 决心评估 EV71 毒力。propidium 碘化物染色的流动 cytometry 分析被执行分析 MRC5 房间的房间周期分发。感冒 emodin (29.6 mol/L ) 有效地保护了 MRC5 房间免受导致 EV71 的 cytopathic 效果的伤害，它源于禁止病毒的复制：感冒 emodin 处理减少了由 5.34 褶层，由不到 30 褶层的病毒的蛋白质表示和由 0.33107 褶层的 EV71 毒力的病毒的 genomic 层次。病毒的毒力上的感冒 emodin 的抑制是比它 genomic 层次和病毒的蛋白质表示上的效果强壮得多的事实建议感冒 emodin 禁止了病毒的成熟。而且，感冒 emodin 处理显著地减少了在 S 的房间周期拘捕在 MRC5 房间分阶段执行，它被 EV71 感染导致并且赞成了病毒的复制。相反，既不 astragaloside (50 mol/L ) 也不 artemisinin (50 mol/L ) 显示出类似的 anti-EV71 活动。在测试的三自然混合物之中，感冒 emodin 有效地压制了 EV71 病毒的复制，因此是候选人 anti-HFMD 药。

英文摘要：

Human enterovirus 71 （EV71） is the primary causative agent of recent large-scale outbreaks of hand, foot, and mouth disease （HFMD） in Asia. Currently, there are no drugs available for the prevention and treatment of HFMD. In this study, we compared the anti-EV71 activities of three natural compounds, rheum emodin, artemisinin and astragaloside extracted from Chinese herbs Chinese rhubarb, Artemisia carvifolia and Astragalus, respectively, which have been traditionally used for the treatment and prevention of epidemic diseases. Human lung fibroblast cell line MRC5 was mock-infected or infected with EV71, and treated with drugs. The cytotoxicity of the drugs was detected with MTT assay. The cytopathic effects such as cell death and condensed nuclei were morphologically observed. The VPl-coding sequence required for EV71 genome replication was assayed with qRT-PCR. Viral protein expression was analyzed with Western blotting. Viral TClD50 was determined to evaluate EV71 virulence. Flow cytometry analysis of propidium iodide staining was performed to analyze the cell cycle distribution of MRC5 cells. Rheum emodin （29.6 pmol/L） effectively protected MRC5 cells from EV71-induced cytopathic effects, which resulted from the inhibiting viral replication： rheum emodin treatment decreased vira genomic levels by 5.34-fold, viral protein expression by less than 30-fold and EV71 virulence by 0.33107-fold. The fact that inhibition of rheum emodin on viral virulence was much stronger than its effects on genomic levels and viral protein expression suggested that rheum emodin inhibited viral maturation. Furthermore, rheum emodin treatment markedly diminished cell cycle arrest at S phase in MRC5 cells, which was induced by EV71 infection and favored the viral replication. In contrast, neither astragaloside （50 pmol/L） nor artemisinin （50 pmol/L） showed similar anti-EV71 activities. Among the three natural compounds tested, rheum emodin effectively suppressed EV71 viral replication, thus is a candidate anti-HFMD