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Sulforaphane Suppresses Hepatitis C Virus Replication by Up-Regulating Heme Oxygenase-1 Expression through PI3K/Nrf2 Pathway.
Yu, Jung-Sheng; Chen, Wei-Chun; Tseng, Chin-Kai; Lin, Chun-Kuang; Hsu, Yao-Chin; Chen, Yen-Hsu; Lee, Jin-Ching.
Afiliación
  • Yu JS; Department of Chinese Medicine, Chi Mei Medical Center, Tainan, 71004, Taiwan.
  • Chen WC; Graduate Institute of Integrated Medicine, China Medical University, Taichung, 40402, Taiwan.
  • Tseng CK; Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
  • Lin CK; Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
  • Hsu YC; Center of Infectious Disease and Signaling Research, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
  • Chen YH; Doctoral Degree Program in Marine Biotechnology, College of Marine Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.
  • Lee JC; Department of Chinese Medicine, Chi Mei Medical Center, Tainan, 71004, Taiwan.
PLoS One ; 11(3): e0152236, 2016.
Article en En | MEDLINE | ID: mdl-27023634
Hepatitis 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 µM. 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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Replicación Viral / Regulación hacia Arriba / Isotiocianatos / Hepacivirus / Fosfatidilinositol 3-Quinasas / Hemo-Oxigenasa 1 / Factor 2 Relacionado con NF-E2 Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2016 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Replicación Viral / Regulación hacia Arriba / Isotiocianatos / Hepacivirus / Fosfatidilinositol 3-Quinasas / Hemo-Oxigenasa 1 / Factor 2 Relacionado con NF-E2 Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2016 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos