Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability

Abstract β-Escin is a mixture of triterpenoid saponins extracted from horse chestnut seeds that have diverse pharmacological activities, including anti-inflammation, anti-edematous, venotonic, and antiviral effects. In the clinical setting, β-escin is primarily used to treat venous insufficiency and...

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Main Authors: Zheng-Zong Lai, Hsin-Hsuen Shen, Yen-Mei Lee
Format: Article
Language:English
Published: Nature Portfolio 2023-06-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-023-36871-1
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author Zheng-Zong Lai
Hsin-Hsuen Shen
Yen-Mei Lee
author_facet Zheng-Zong Lai
Hsin-Hsuen Shen
Yen-Mei Lee
author_sort Zheng-Zong Lai
collection DOAJ
description Abstract β-Escin is a mixture of triterpenoid saponins extracted from horse chestnut seeds that have diverse pharmacological activities, including anti-inflammation, anti-edematous, venotonic, and antiviral effects. In the clinical setting, β-escin is primarily used to treat venous insufficiency and blunt trauma injuries. The anti-Zika virus (ZIKV) activity of β-escin has not been explored. This study investigated the antiviral efficacy of β-escin on ZIKV and dengue virus (DENV) in vitro and then elucidated the underlying mechanism. The inhibitory effects of β-escin on viral RNA synthesis, protein levels, and infection ability were determined using qRT-PCR, Western blotting, and immunofluorescence assays, respectively. To further characterize how β-escin interferes with the viral life cycle, the time-of-addition experiment was performed. An inactivation assay was performed to determine whether β-escin affects ZIKV virion stability. To broaden these findings, the antiviral effects of β-escin on different DENV serotypes were assessed using dose-inhibition and time-of-addition assays. The results showed that β-escin exhibits anti-ZIKV activity by decreasing viral RNA levels, protein expression, progeny yield, and virion stability. β-Escin inhibited ZIKV infection by disrupting viral binding and replication. Furthermore, β-escin demonstrated antiviral activities against four DENV serotypes in a Vero cell model and prophylactic protection against ZIKV and DENV infections.
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spelling doaj.art-a69878416e1f4f05a458be7a94a6e3992023-06-25T11:17:13ZengNature PortfolioScientific Reports2045-23222023-06-0113111010.1038/s41598-023-36871-1Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stabilityZheng-Zong Lai0Hsin-Hsuen Shen1Yen-Mei Lee2Graduate Institute of Medical Science, National Defense Medical CenterDepartment and Graduate Institute of Pharmacology, National Defense Medical CenterDepartment and Graduate Institute of Pharmacology, National Defense Medical CenterAbstract β-Escin is a mixture of triterpenoid saponins extracted from horse chestnut seeds that have diverse pharmacological activities, including anti-inflammation, anti-edematous, venotonic, and antiviral effects. In the clinical setting, β-escin is primarily used to treat venous insufficiency and blunt trauma injuries. The anti-Zika virus (ZIKV) activity of β-escin has not been explored. This study investigated the antiviral efficacy of β-escin on ZIKV and dengue virus (DENV) in vitro and then elucidated the underlying mechanism. The inhibitory effects of β-escin on viral RNA synthesis, protein levels, and infection ability were determined using qRT-PCR, Western blotting, and immunofluorescence assays, respectively. To further characterize how β-escin interferes with the viral life cycle, the time-of-addition experiment was performed. An inactivation assay was performed to determine whether β-escin affects ZIKV virion stability. To broaden these findings, the antiviral effects of β-escin on different DENV serotypes were assessed using dose-inhibition and time-of-addition assays. The results showed that β-escin exhibits anti-ZIKV activity by decreasing viral RNA levels, protein expression, progeny yield, and virion stability. β-Escin inhibited ZIKV infection by disrupting viral binding and replication. Furthermore, β-escin demonstrated antiviral activities against four DENV serotypes in a Vero cell model and prophylactic protection against ZIKV and DENV infections.https://doi.org/10.1038/s41598-023-36871-1
spellingShingle Zheng-Zong Lai
Hsin-Hsuen Shen
Yen-Mei Lee
Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability
Scientific Reports
title Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability
title_full Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability
title_fullStr Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability
title_full_unstemmed Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability
title_short Inhibitory effect of β-escin on Zika virus infection through the interruption of viral binding, replication, and stability
title_sort inhibitory effect of β escin on zika virus infection through the interruption of viral binding replication and stability
url https://doi.org/10.1038/s41598-023-36871-1
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AT yenmeilee inhibitoryeffectofbescinonzikavirusinfectionthroughtheinterruptionofviralbindingreplicationandstability