Fucoidan from Fucus vesiculosus suppresses hepatitis B virus replication by enhancing extracellular signal-regulated Kin
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RESEARCH
Open Access
Fucoidan from Fucus vesiculosus suppresses hepatitis B virus replication by enhancing extracellular signal-regulated Kinase activation Huifang Li1, Junru Li1, Yuan Tang1, Lin Lin1,2, Zhanglian Xie3, Jia Zhou1, Liyun Zhang1, Xiaoyong Zhang3, Xiaoshan Zhao4, Zhengliang Chen1,5 and Daming Zuo1,5*
Abstract Background: Hepatitis B virus (HBV) infection is a serious public health problem leading to cirrhosis and hepatocellular carcinoma. As the clinical utility of current therapies is limited, the development of new therapeutic approaches for the prevention and treatment of HBV infection is imperative. Fucoidan is a natural sulfated polysaccharide that extracted from different species of brown seaweed, which was reported to exhibit various bioactivities. However, it remains unclear whether fucoidan influences HBV replication or not. Methods: The HBV-infected mouse model was established by hydrodynamic injection of HBV replicative plasmid, and the mice were treated with saline or fucoidan respectively. Besides, we also tested the inhibitory effect of fucoidan against HBV infection in HBV-transfected cell lines. Results: The result showed that fucoidan from Fucus vesiculosus decreased serum HBV DNA, HBsAg and HBeAg levels and hepatic HBcAg expression in HBV-infected mice. Moreover, fucoidan treatment also suppressed intracellular HBcAg expression and the secretion of the HBV DNA as well as HBsAg and HBeAg in HBV-expressing cells. Furthermore, we proved that the inhibitory activity by fucoidan was due to the activation of the extracellular signal-regulated kinase (ERK) pathway and the subsequent production of type I interferon. Using specific inhibitor of ERK pathway abrogated the fucoidan-mediated inhibition of HBV replication. Conclusion: This study highlights that fucoidan might be served as an alternative therapeutic approach for the treatment of HBV infection. Keywords: Fucoidan, Hepatitis B virus, Extracellular signal-regulated kinase, Interferon, Anti-viral effect
Background Hepatitis B virus (HBV) infection is a global public health problem. The infection can lead to acute and chronic hepatitis, which makes liver prone to develop cirrhosis and hepatocellular carcinoma [1]. Although an effective vaccine has been used for 20 years in many countries, there are still about 350 million chronic carriers of HBV worldwide, and approximately 1 million people die from * Correspondence: [email protected] 1 Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China 5 Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, Guangdong 510515, China Full list of author information is available at the end of the article
HBV-related liver diseases each year [2]. The currently approved agents for the treatment of HBV infection include immunomodulatory agents, such as interferon-α (IFN-α) and pegylated IFN-α, and oral nucleoside/nucleotide analogues, like lamivudine, adefovir, telbivudine, entecavir and tenofov
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