Anti-HBV activity and mechanism of marine-derived polyguluronate sulfate (PGS) in vitro. (5th June 2016)

• Record Type: Journal Article
• Authors: Wu, Lijuan; Wang, Wei; Zhang, Xiaoshuang; Zhao, Xia; Yu, Guangli
• Is Part Of: Carbohydrate polymers. Volume 143(2016)
• Page Start: 139
• Page End: 148
• Publication Date: 2016-06-05
• Subjects: 3TC lamivudine -- CC50 concentration of 50% cytotoxicity -- DP degree of polymerization -- ELISA enzyme-linked immunosorbent assay -- FCM flow cytometry -- HBeAg HBV e antigen -- HBsAg HBV surface antigen -- HBV hepatitis B virus -- HNF4α hepatocyte nuclear factor 4α -- IFN-β interferon beta -- MAPK mitogen-activated protein kinases -- MTT 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide -- NF-κB nuclear factor-kappa B -- PGS Polyguluronate sulfate; Polyguluronate sulfate -- Hepatitis B virus -- Anti-viral activity -- Interferon -- Raf/MEK/ERK pathway; Polysaccharides -- Periodicals; Polysaccharides -- Periodicals; Polysaccharides -- Périodiques; Electronic journals; 547.78
• DOI: 10.1016/j.carbpol.2016.01.065
• Languages: English
• ISSNs: 0144-8617

Abstract

Highlights: Polyguluronate sulfate (PGS) effectively inhibits HBV replication in HepG2.2.15 cells. PGS inhibited the expression and secretion of HBsAg and HBeAg with low cytotoxicity. PGS can bind and enter into HepG2.2.15 cells to interfere with HBV transcription. PGS can enhance the production and secretion of interferon β in HepG2.2.15 cells. PGS may upregulate NF-κB and Raf/MEK/ERK pathways to enhance the interferon system. Abstract: Polyguluronate sulfate (PGS) is a low molecular-weight sulfated derivative, which has a structure of 2, 3-O-disulfated-1, 4-poly-l -guluronic acid (PG) with about 1.5 sulfate per sugar residue. Herein, our results showed that PGS effectively inhibited the expression and secretion of HBsAg and HBeAg in HepG2.2.15 cells. PGS could bind and enter into HepG2.2.15 cells to interfere with HBV transcription rather than blocking HBV DNA replication. Moreover, PGS also enhanced the production and secretion of interferon beta (IFN-β) in HepG2.2.15 cells. Cellular NF-κB and Raf/MEK/ERK signaling pathways were also involved in the anti-HBV actions of PGS. Thus, PGS may inhibit HBV replication through upregulating the NF-κB and Raf/MEK/ERK pathways to enhance the interferon system. In summary, PGS merits further investigation as a novel anti-HBV agent aimed at modulating the host innate immune system in the future.