Thujaplicin–copper chelates inhibit replication of human influenza viruses
Identifieur interne : 000197 ( Istex/Curation ); précédent : 000196; suivant : 000198Thujaplicin–copper chelates inhibit replication of human influenza viruses
Auteurs : Daisei Miyamoto [Japon] ; Yuki Kusagaya [Japon] ; Naoko Endo [Japon] ; Ayako Sometani [Japon] ; Seiji Takeo [Japon] ; Takashi Suzuki [Japon] ; Yaeno Arima [Japon] ; Katsuyuki Nakajima [États-Unis] ; Yasuo Suzuki [Japon]Source :
- Antiviral Research [ 0166-3542 ] ; 1998.
English descriptors
- Teeft :
- Anti6iral, Anti6iral research, Apoptosis, Apoptotic, Assay, Canine kidney, Cell death, Cell growth, Cell viability, Chelate, Chem, Copper chelate, Copper chelates, Copper ions, Copper sulfate, Culture medium, Cytometric, Cytometric analysis, Cytotoxic, Cytotoxic effects, Early phase, Early stage, Hela cells, Host cells, Human apoptosis, Inhibitory effects, Lactate dehydrogenase, Mdck, Mdck cells, Metal chelates, Miyamoto, Morphological changes, Postinfection, Supernatant, Suzuki, Takizawa, Test samples, Thuja plicata, Thujaplicin, Thujaplicin copper chelates, Thujaplicins, Total cells, Viral, Viral infection, Virus, Virus infection, Zinc ions.
Abstract
Abstract: The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin–Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin–copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2–4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin–copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.
Url:
DOI: 10.1016/S0166-3542(98)00034-5
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<term>Anti6iral research</term>
<term>Apoptosis</term>
<term>Apoptotic</term>
<term>Assay</term>
<term>Canine kidney</term>
<term>Cell death</term>
<term>Cell growth</term>
<term>Cell viability</term>
<term>Chelate</term>
<term>Chem</term>
<term>Copper chelate</term>
<term>Copper chelates</term>
<term>Copper ions</term>
<term>Copper sulfate</term>
<term>Culture medium</term>
<term>Cytometric</term>
<term>Cytometric analysis</term>
<term>Cytotoxic</term>
<term>Cytotoxic effects</term>
<term>Early phase</term>
<term>Early stage</term>
<term>Hela cells</term>
<term>Host cells</term>
<term>Human apoptosis</term>
<term>Inhibitory effects</term>
<term>Lactate dehydrogenase</term>
<term>Mdck</term>
<term>Mdck cells</term>
<term>Metal chelates</term>
<term>Miyamoto</term>
<term>Morphological changes</term>
<term>Postinfection</term>
<term>Supernatant</term>
<term>Suzuki</term>
<term>Takizawa</term>
<term>Test samples</term>
<term>Thuja plicata</term>
<term>Thujaplicin</term>
<term>Thujaplicin copper chelates</term>
<term>Thujaplicins</term>
<term>Total cells</term>
<term>Viral</term>
<term>Viral infection</term>
<term>Virus</term>
<term>Virus infection</term>
<term>Zinc ions</term>
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<front><div type="abstract" xml:lang="en">Abstract: The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin–Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin–copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2–4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin–copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.</div>
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