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dc.contributor.authorYu, Jung-Shengen_US
dc.contributor.authorChen, Wei-Chunen_US
dc.contributor.authorTseng, Chin-Kaien_US
dc.contributor.authorLin, Chun-Kuangen_US
dc.contributor.authorHsu, Yao-Chinen_US
dc.contributor.authorChen, Yen-Hsuen_US
dc.contributor.authorLee, Jin-Chingen_US
dc.date.accessioned2019-04-03T06:42:12Z-
dc.date.available2019-04-03T06:42:12Z-
dc.date.issued2016-03-29en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://dx.doi.org/10.1371/journal.pone.0152236en_US
dc.identifier.urihttp://hdl.handle.net/11536/133462-
dc.description.abstractHepatitis C virus (HCV) infection-induced oxidative stress is a major risk factor for the development of HCV-associated liver disease. Sulforaphane (SFN) is an antioxidant phytocompound that acts against cellular oxidative stress and tumorigenesis. However, there is little known about its anti-viral activity. In this study, we demonstrated that SFN significantly suppressed HCV protein and RNA levels in HCV replicon cells and infectious system, with an IC50 value of 5.7 +/- 0.2 mu M. Moreover, combination of SFN with anti-viral drugs displayed synergistic effects in the suppression of HCV replication. In addition, we found nuclear factor erythroid 2-related factor 2 (Nrf2)/HO-1 induction in response to SFN and determined the signaling pathways involved in this process, including inhibition of NS3 protease activity and induction of IFN response. In contrast, the anti-viral activities were attenuated by knockdown of HO-1 with specific inhibitor (SnPP) and shRNA, suggesting that anti-HCV activity of SFN is dependent on HO-1 expression. Otherwise, SFN stimulated the phosphorylation of phosphoinositide 3-kinase (PI3K) leading Nrf2-mediated HO-1 expression against HCV replication. Overall, our results indicated that HO-1 is essential in SFN-mediated anti-HCV activity and provide new insights in the molecular mechanism of SFN in HCV replication.en_US
dc.language.isoen_USen_US
dc.titleSulforaphane Suppresses Hepatitis C Virus Replication by Up-Regulating Heme Oxygenase-1 Expression through PI3K/Nrf2 Pathwayen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0152236en_US
dc.identifier.journalPLOS ONEen_US
dc.citation.volume11en_US
dc.citation.issue3en_US
dc.citation.spage0en_US
dc.citation.epage0en_US
dc.contributor.department生醫工程研究所zh_TW
dc.contributor.departmentInstitute of Biomedical Engineeringen_US
dc.identifier.wosnumberWOS:000373113900033en_US
dc.citation.woscount6en_US
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