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腾讯登录JBC：姜黄素阻止病毒在人细胞中复制
| 导读 | 美国乔治梅森大学研究人员最近发现，最为流行的香料姜黄(turmeric)不只是充满气味，而且它还有望抵抗破坏性的病毒。相关研究论文发表在<em>Journal of Biological Chemistry</em>期刊上。
论文第一作者、乔治梅森大学国家生物防御与传染病中心研究助理教授Aarthi Narayanan说，在姜黄中发现的姜黄素(curcumin)阻止潜... |
美国乔治梅森大学研究人员最近发现，最为流行的香料姜黄(turmeric)不只是充满气味，而且它还有望抵抗破坏性的病毒。相关研究论文发表在<em>Journal of Biological Chemistry</em>期刊上。
论文第一作者、乔治梅森大学国家生物防御与传染病中心研究助理教授Aarthi Narayanan说，在姜黄中发现的姜黄素(curcumin)阻止潜在致命性的裂谷热病毒(Rift Valley Fever virus, RVFV)在被它感染的细胞中增殖。
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蚊子传播的裂谷热病毒(RVFV)是一种急性的导致导致发热的病毒，能够影响诸如牛、绵羊和山羊之类家畜和人。
Narayanan强调，在基于姜黄素的药物变得司空见惯之前，还有更多的研究需要开展。她计划测试10种不同的姜黄素版本以便确定哪个效果最佳。
究其本质而言，姜黄素是一种广谱的阻止一系列病毒感染健康细胞的抑制剂。但是在这篇论文中，研究人员证实姜黄素可能干扰RVFV操纵人细胞从而阻止细胞对感染作出反应。他们发现姜黄素不仅在体外细胞培养物中显著性地抑制RVFV复制，而且也在小鼠模式动物中证实它能够有效地对抗RVFV感染。
一旦人们知道身体如何对一种病毒作出反应，那么科学家们就有时间对抗这种病毒。Narayanan正在利用这种知识到布尼亚病毒、委内瑞拉马脑炎病毒和包括在HIV在内的逆转录病毒。
本文编译自<a href="http://phys.org/news/2012-08-turmeric-spices-virus-curcumin-cells.html" target="_blank">Turmeric spices up virus study: New research shows curcumin stops virus cells</a>
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<a title="" href="http://dx.doi.org/10.1074/jbc.M112.356535" target="_blank">doi: 10.1074/jbc.M112.356535</a>
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<br/><strong>Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells</strong><br/>
Aarthi Narayanan1, Kylene Kehn-Hall1, Svetlana Senina1, Lindsay Hill1, Rachel Van Duyne2, Irene Guendel1, Ravi Das1, Alan Baer1, Laura Bethel3, Michael Turrell4, Amy Lynn Hartman3, Bhaskar Das5, Charles Bailey1 and Fatah Kashanchi
Rift Valley fever virus (RVFV) is an arbovirus that is classified as a select agent, an emerging infectious virus and an agricultural pathogen. Understanding RVFV-host interactions is imperative to the design of novel therapeutics. Here, we report that an infection by the MP-12 strain of RVFV induces phosphorylation of the p65 component of the NFκB cascade. We demonstrate that phosphorylation of p65 (serine 536) involves phosphorylation of IκBα and occurs through the classical NFκB cascade. A unique low molecular weight complex of the IKK-β subunit can be observed in MP-12 infected cells that we have labeled as IKK-β2. The IKK-β2 complex retains kinase activity and phosphorylates an IκBα substrate. Inhibition of the IKK complex using inhibitors impairs viral replication thus alluding to the requirement of an active IKK complex to the viral life cycle. Curcumin, strongly down regulates levels of extracellular infectious virus. Our data demonstrate that curcumin binds to and inhibits kinase activity of the IKK-β2 complex in infected cells. Curcumin partially exerts its inhibitory influence on RVFV replication by interfering with IKK-β2 mediated phosphorylation of the viral protein NSs and by altering cell cycle of treated cells. Curcumin also demonstrates efficacy against ZH501, the fully virulent version of RVFV. Curcumin treatment down regulates viral replication in the liver of infected animals. Our data point to the possibility that RVFV infection may result in the generation of novel versions of host components (such as IKK-β2) that by virtue of altered protein interaction and function, qualify as unique therapeutic targets.
<br/>来源：生物谷
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论文第一作者、乔治梅森大学国家生物防御与传染病中心研究助理教授Aarthi Narayanan说，在姜黄中发现的姜黄素(curcumin)阻止潜在致命性的裂谷热病毒(Rift Valley Fever virus, RVFV)在被它感染的细胞中增殖。
<!--more-->
蚊子传播的裂谷热病毒(RVFV)是一种急性的导致导致发热的病毒，能够影响诸如牛、绵羊和山羊之类家畜和人。
Narayanan强调，在基于姜黄素的药物变得司空见惯之前，还有更多的研究需要开展。她计划测试10种不同的姜黄素版本以便确定哪个效果最佳。
究其本质而言，姜黄素是一种广谱的阻止一系列病毒感染健康细胞的抑制剂。但是在这篇论文中，研究人员证实姜黄素可能干扰RVFV操纵人细胞从而阻止细胞对感染作出反应。他们发现姜黄素不仅在体外细胞培养物中显著性地抑制RVFV复制，而且也在小鼠模式动物中证实它能够有效地对抗RVFV感染。
一旦人们知道身体如何对一种病毒作出反应，那么科学家们就有时间对抗这种病毒。Narayanan正在利用这种知识到布尼亚病毒、委内瑞拉马脑炎病毒和包括在HIV在内的逆转录病毒。
本文编译自<a href="http://phys.org/news/2012-08-turmeric-spices-virus-curcumin-cells.html" target="_blank">Turmeric spices up virus study: New research shows curcumin stops virus cells</a>
<div id="ztload">
<div> </div>
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201208/2012081912350490.gif" alt="" width="113" height="149" border="0" />
<a title="" href="http://dx.doi.org/10.1074/jbc.M112.356535" target="_blank">doi: 10.1074/jbc.M112.356535</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells</strong><br/>
Aarthi Narayanan1, Kylene Kehn-Hall1, Svetlana Senina1, Lindsay Hill1, Rachel Van Duyne2, Irene Guendel1, Ravi Das1, Alan Baer1, Laura Bethel3, Michael Turrell4, Amy Lynn Hartman3, Bhaskar Das5, Charles Bailey1 and Fatah Kashanchi
Rift Valley fever virus (RVFV) is an arbovirus that is classified as a select agent, an emerging infectious virus and an agricultural pathogen. Understanding RVFV-host interactions is imperative to the design of novel therapeutics. Here, we report that an infection by the MP-12 strain of RVFV induces phosphorylation of the p65 component of the NFκB cascade. We demonstrate that phosphorylation of p65 (serine 536) involves phosphorylation of IκBα and occurs through the classical NFκB cascade. A unique low molecular weight complex of the IKK-β subunit can be observed in MP-12 infected cells that we have labeled as IKK-β2. The IKK-β2 complex retains kinase activity and phosphorylates an IκBα substrate. Inhibition of the IKK complex using inhibitors impairs viral replication thus alluding to the requirement of an active IKK complex to the viral life cycle. Curcumin, strongly down regulates levels of extracellular infectious virus. Our data demonstrate that curcumin binds to and inhibits kinase activity of the IKK-β2 complex in infected cells. Curcumin partially exerts its inhibitory influence on RVFV replication by interfering with IKK-β2 mediated phosphorylation of the viral protein NSs and by altering cell cycle of treated cells. Curcumin also demonstrates efficacy against ZH501, the fully virulent version of RVFV. Curcumin treatment down regulates viral replication in the liver of infected animals. Our data point to the possibility that RVFV infection may result in the generation of novel versions of host components (such as IKK-β2) that by virtue of altered protein interaction and function, qualify as unique therapeutic targets.
<br/>来源：生物谷
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