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小白菊内酯体外影响单纯疱疹病毒 1 复制。

Parthenolide Influences Herpes simplex virus 1 Replication in vitro.

机构信息

Postgraduate Program in Pharmaceutical Sciences, State University of Maringá, Maringá, Brazil.

Department of Basic Health Sciences, State University of Maringá, Maringá, Brazil.

出版信息

Intervirology. 2018;61(1):14-22. doi: 10.1159/000490055. Epub 2018 Jul 12.

DOI:10.1159/000490055
PMID:30001535
Abstract

BACKGROUND/AIMS: Parthenolide is a sesquiterpene lactone that is present in plants of the Tanacetum genus, for which many biological effects have already been reported, including antiherpetic activity. Although the effectiveness of parthenolide against Herpes simplex virus 1 (HSV-1) has already been demonstrated, such findings are still controversial. The objective of this study was to investigate the ways in which parthenolide exerts anti-HSV-1 activity.

METHODS

The cytotoxicity and antiviral activity of parthenolide were determined by the MTT method and plaque reduction assay, respectively. The expression of cell and viral proteins during the treatment of infected cells was investigated by Western blot.

RESULTS

Both strains of HSV-1 were sensitive to parthenolide, and parthenolide was active only after penetration of the virus into the host cell. The expression of p65 protein decreased, the expression of caspases 8 and 9 increased, and the expression of c-Jun N-terminal kinase (JNK) and p38 protein was altered in infected cells after parthenolide treatment, resulting in lower cell survival. The low expression of viral proteins gB, gD, and ICP0 confirmed the reduction of HSV-1 particle production.

CONCLUSION

Parthenolide exerts anti-HSV-1 activity by impairing cell viability, which consequently interferes with the efficient infection and production of new viral particles.

摘要

背景/目的:小白菊内酯是一种倍半萜内酯,存在于菊科植物中,已有许多生物效应被报道,包括抗疱疹活性。虽然小白菊内酯对单纯疱疹病毒 1(HSV-1)的有效性已经得到证实,但这些发现仍存在争议。本研究旨在探讨小白菊内酯发挥抗 HSV-1 活性的方式。

方法

通过 MTT 法和蚀斑减少试验分别测定小白菊内酯的细胞毒性和抗病毒活性。通过 Western blot 检测感染细胞治疗过程中细胞和病毒蛋白的表达。

结果

两种 HSV-1 株均对小白菊内酯敏感,小白菊内酯仅在病毒进入宿主细胞后才具有活性。感染细胞经小白菊内酯处理后,p65 蛋白表达降低,caspases 8 和 9 表达增加,c-Jun N-末端激酶(JNK)和 p38 蛋白表达改变,导致细胞存活率降低。病毒蛋白 gB、gD 和 ICP0 的低表达证实了 HSV-1 颗粒产生的减少。

结论

小白菊内酯通过损害细胞活力发挥抗 HSV-1 活性,从而干扰病毒粒子的有效感染和产生。

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