Curcumin inhibits the replication of enterovirus 71 in vitro

Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Ying Qin [verfasserIn] Lexun Lin [verfasserIn] Yang Chen [verfasserIn] Shuo Wu [verfasserIn] Xiaoning Si [verfasserIn] Heng Wu [verfasserIn] Xia Zhai [verfasserIn] Yan Wang [verfasserIn] Lei Tong [verfasserIn] Bo Pan [verfasserIn] Xiaoyan Zhong [verfasserIn] Tianying Wang [verfasserIn] Wenran Zhao [verfasserIn] Zhaohua Zhong [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis

Übergeordnetes Werk:	In: Acta Pharmaceutica Sinica B - Elsevier, 2013, 4(2014), 4, Seite 284-294
Übergeordnetes Werk:	volume:4 ; year:2014 ; number:4 ; pages:284-294

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1016/j.apsb.2014.06.006

Katalog-ID:	DOAJ057381186

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520			\|a Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies.
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allfields	10.1016/j.apsb.2014.06.006 doi (DE-627)DOAJ057381186 (DE-599)DOAJ723ddc80504743a4a44905f654c2ce6b DE-627 ger DE-627 rakwb eng RM1-950 Ying Qin verfasserin aut Curcumin inhibits the replication of enterovirus 71 in vitro 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies. Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis Therapeutics. Pharmacology Lexun Lin verfasserin aut Yang Chen verfasserin aut Shuo Wu verfasserin aut Xiaoning Si verfasserin aut Heng Wu verfasserin aut Xia Zhai verfasserin aut Yan Wang verfasserin aut Lei Tong verfasserin aut Bo Pan verfasserin aut Xiaoyan Zhong verfasserin aut Tianying Wang verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 4(2014), 4, Seite 284-294 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:4 year:2014 number:4 pages:284-294 https://doi.org/10.1016/j.apsb.2014.06.006 kostenfrei https://doaj.org/article/723ddc80504743a4a44905f654c2ce6b kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383514000586 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei https://doaj.org/toc/2211-3843 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2014 4 284-294
spelling	10.1016/j.apsb.2014.06.006 doi (DE-627)DOAJ057381186 (DE-599)DOAJ723ddc80504743a4a44905f654c2ce6b DE-627 ger DE-627 rakwb eng RM1-950 Ying Qin verfasserin aut Curcumin inhibits the replication of enterovirus 71 in vitro 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies. Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis Therapeutics. Pharmacology Lexun Lin verfasserin aut Yang Chen verfasserin aut Shuo Wu verfasserin aut Xiaoning Si verfasserin aut Heng Wu verfasserin aut Xia Zhai verfasserin aut Yan Wang verfasserin aut Lei Tong verfasserin aut Bo Pan verfasserin aut Xiaoyan Zhong verfasserin aut Tianying Wang verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 4(2014), 4, Seite 284-294 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:4 year:2014 number:4 pages:284-294 https://doi.org/10.1016/j.apsb.2014.06.006 kostenfrei https://doaj.org/article/723ddc80504743a4a44905f654c2ce6b kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383514000586 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei https://doaj.org/toc/2211-3843 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2014 4 284-294
allfields_unstemmed	10.1016/j.apsb.2014.06.006 doi (DE-627)DOAJ057381186 (DE-599)DOAJ723ddc80504743a4a44905f654c2ce6b DE-627 ger DE-627 rakwb eng RM1-950 Ying Qin verfasserin aut Curcumin inhibits the replication of enterovirus 71 in vitro 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies. Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis Therapeutics. Pharmacology Lexun Lin verfasserin aut Yang Chen verfasserin aut Shuo Wu verfasserin aut Xiaoning Si verfasserin aut Heng Wu verfasserin aut Xia Zhai verfasserin aut Yan Wang verfasserin aut Lei Tong verfasserin aut Bo Pan verfasserin aut Xiaoyan Zhong verfasserin aut Tianying Wang verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 4(2014), 4, Seite 284-294 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:4 year:2014 number:4 pages:284-294 https://doi.org/10.1016/j.apsb.2014.06.006 kostenfrei https://doaj.org/article/723ddc80504743a4a44905f654c2ce6b kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383514000586 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei https://doaj.org/toc/2211-3843 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2014 4 284-294
allfieldsGer	10.1016/j.apsb.2014.06.006 doi (DE-627)DOAJ057381186 (DE-599)DOAJ723ddc80504743a4a44905f654c2ce6b DE-627 ger DE-627 rakwb eng RM1-950 Ying Qin verfasserin aut Curcumin inhibits the replication of enterovirus 71 in vitro 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies. Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis Therapeutics. Pharmacology Lexun Lin verfasserin aut Yang Chen verfasserin aut Shuo Wu verfasserin aut Xiaoning Si verfasserin aut Heng Wu verfasserin aut Xia Zhai verfasserin aut Yan Wang verfasserin aut Lei Tong verfasserin aut Bo Pan verfasserin aut Xiaoyan Zhong verfasserin aut Tianying Wang verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 4(2014), 4, Seite 284-294 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:4 year:2014 number:4 pages:284-294 https://doi.org/10.1016/j.apsb.2014.06.006 kostenfrei https://doaj.org/article/723ddc80504743a4a44905f654c2ce6b kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383514000586 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei https://doaj.org/toc/2211-3843 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2014 4 284-294
allfieldsSound	10.1016/j.apsb.2014.06.006 doi (DE-627)DOAJ057381186 (DE-599)DOAJ723ddc80504743a4a44905f654c2ce6b DE-627 ger DE-627 rakwb eng RM1-950 Ying Qin verfasserin aut Curcumin inhibits the replication of enterovirus 71 in vitro 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies. Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis Therapeutics. Pharmacology Lexun Lin verfasserin aut Yang Chen verfasserin aut Shuo Wu verfasserin aut Xiaoning Si verfasserin aut Heng Wu verfasserin aut Xia Zhai verfasserin aut Yan Wang verfasserin aut Lei Tong verfasserin aut Bo Pan verfasserin aut Xiaoyan Zhong verfasserin aut Tianying Wang verfasserin aut Wenran Zhao verfasserin aut Zhaohua Zhong verfasserin aut In Acta Pharmaceutica Sinica B Elsevier, 2013 4(2014), 4, Seite 284-294 (DE-627)670211095 (DE-600)2631779-5 22113843 nnns volume:4 year:2014 number:4 pages:284-294 https://doi.org/10.1016/j.apsb.2014.06.006 kostenfrei https://doaj.org/article/723ddc80504743a4a44905f654c2ce6b kostenfrei http://www.sciencedirect.com/science/article/pii/S2211383514000586 kostenfrei https://doaj.org/toc/2211-3835 Journal toc kostenfrei https://doaj.org/toc/2211-3843 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2014 4 284-294
language	English
source	In Acta Pharmaceutica Sinica B 4(2014), 4, Seite 284-294 volume:4 year:2014 number:4 pages:284-294
sourceStr	In Acta Pharmaceutica Sinica B 4(2014), 4, Seite 284-294 volume:4 year:2014 number:4 pages:284-294
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Acta Pharmaceutica Sinica B
authorswithroles_txt_mv	Ying Qin @@aut@@ Lexun Lin @@aut@@ Yang Chen @@aut@@ Shuo Wu @@aut@@ Xiaoning Si @@aut@@ Heng Wu @@aut@@ Xia Zhai @@aut@@ Yan Wang @@aut@@ Lei Tong @@aut@@ Bo Pan @@aut@@ Xiaoyan Zhong @@aut@@ Tianying Wang @@aut@@ Wenran Zhao @@aut@@ Zhaohua Zhong @@aut@@
publishDateDaySort_date	2014-01-01T00:00:00Z
hierarchy_top_id	670211095
id	DOAJ057381186
language_de	englisch
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callnumber-first	R - Medicine
author	Ying Qin
spellingShingle	Ying Qin misc RM1-950 misc Curcumin misc Enterovirus 71 misc Viral replication misc GBF1 misc PI4KB misc Ubiquitin–proteasome system misc Apoptosis misc Therapeutics. Pharmacology Curcumin inhibits the replication of enterovirus 71 in vitro
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topic_title	RM1-950 Curcumin inhibits the replication of enterovirus 71 in vitro Curcumin Enterovirus 71 Viral replication GBF1 PI4KB Ubiquitin–proteasome system Apoptosis
topic	misc RM1-950 misc Curcumin misc Enterovirus 71 misc Viral replication misc GBF1 misc PI4KB misc Ubiquitin–proteasome system misc Apoptosis misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc Curcumin misc Enterovirus 71 misc Viral replication misc GBF1 misc PI4KB misc Ubiquitin–proteasome system misc Apoptosis misc Therapeutics. Pharmacology
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title	Curcumin inhibits the replication of enterovirus 71 in vitro
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title_full	Curcumin inhibits the replication of enterovirus 71 in vitro
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author_browse	Ying Qin Lexun Lin Yang Chen Shuo Wu Xiaoning Si Heng Wu Xia Zhai Yan Wang Lei Tong Bo Pan Xiaoyan Zhong Tianying Wang Wenran Zhao Zhaohua Zhong
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title_sort	curcumin inhibits the replication of enterovirus 71 in vitro
callnumber	RM1-950
title_auth	Curcumin inhibits the replication of enterovirus 71 in vitro
abstract	Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies.
abstractGer	Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies.
abstract_unstemmed	Human enterovirus 71 (EV71) is the main causative pathogen of hand, foot, and mouth disease (HFMD) in children. The epidemic of HFMD has been a public health problem in Asia-Pacific region for decades, and no vaccine and effective antiviral medicine are available. Curcumin has been used as a traditional medicine for centuries to treat a diversity of disorders including viral infections. In this study, we demonstrated that curcumin showed potent antiviral effect again EV71. In Vero cells infected with EV71, the addition of curcumin significantly suppressed the synthesis of viral RNA, the expression of viral protein, and the overall production of viral progeny. Similar with the previous reports, curcumin reduced the production of ROS induced by viral infection. However, the antioxidant property of curcumin did not contribute to its antiviral activity, since N-acetyl-l-cysteine, the potent antioxidant failed to suppress viral replication. This study also showed that extracellular signal-regulated kinase (ERK) was activated by either viral infection or curcumin treatment, but the activated ERK did not interfere with the antiviral effect of curcumin, indicating ERK is not involved in the antiviral mechanism of curcumin. Unlike the previous reports that curcumin inhibited protein degradation through ubiquitin–proteasome system (UPS), we found that curcumin had no impact on UPS in control cells. However, curcumin did reduce the activity of proteasomes which was increased by viral infection. In addition, the accumulation of the short-lived proteins, p53 and p21, was increased by the treatment of curcumin in EV71-infected cells. We further probed the antiviral mechanism of curcumin by examining the expression of GBF1 and PI4KB, both of which are required for the formation of viral replication complex. We found that curcumin significantly reduced the level of both proteins. Moreover, the decreased expression of either GBF1 or PI4KB by the application of siRNAs was sufficient to suppress viral replication. We also demonstrated that curcumin showed anti-apoptotic activity at the early stage of viral infection. The results of this study provide solid evidence that curcumin has potent anti-EV71 activity. Whether or not the down-regulated GBF1 and PI4KB by curcumin contribute to its antiviral effect needs further studies.
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title_short	Curcumin inhibits the replication of enterovirus 71 in vitro
url	https://doi.org/10.1016/j.apsb.2014.06.006 https://doaj.org/article/723ddc80504743a4a44905f654c2ce6b http://www.sciencedirect.com/science/article/pii/S2211383514000586 https://doaj.org/toc/2211-3835 https://doaj.org/toc/2211-3843
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