Co-reporter:Miaomiao Wang, Shuyao Wang, Wei Wang, Yi Wang, Hui Wang, Weiming Zhu
Antiviral Research 2017 Volume 143(Volume 143) pp:
Publication Date(Web):1 July 2017
DOI:10.1016/j.antiviral.2017.04.007
•PPQ-B suppressed IAV replication in vitro with low toxicity, and possessed broad-spectrum anti-IAV activities.•PPQ-B's antiviral activity may be largely related to its inhibition of some steps that occur 0–4 h after adsorption.•Oral administration of PPQ-B decreased pulmonary viral titers and improved survival rate in IAV infected mice.•PPQ-B may down-regulate NF-κB and MAPK signaling pathways to inhibit virus replication.Development of anti-influenza A virus (IAV) drugs with novel targets and low toxicity is critical for preparedness against influenza outbreaks. In the current study, our results indicated that the novel polyketide compound purpurquinone B (PPQ-B) derived from acid-tolerant fungus Penicillium purpurogenum strain JS03-21 suppressed the replication of IAV in vitro with low toxicity, and may block some stages after virus adsorption. PPQ-B could inhibit H1N1 (A/Puerto Rico/8/34; PR8), H1N1 (A/California/04/2009; Cal09) and H3N2 (A/swine/Minnesota/02719/2009) virus replication in vitro, suggesting that PPQ-B possesses broad-spectrum anti-IAV activities. PPQ-B's antiviral activity may be largely related to its inhibition of some steps that occur 0–4 h after adsorption. Oral administration of PPQ-B could decrease pulmonary viral titers and improve survival rate in IAV infected mice. PPQ-B also significantly decreased the production of inflammatory factors TNF-α, IL-6, RANTES and KC in IAV infected lungs and A549 cells, suggesting that PPQ-B may also attenuate the inflammatory responses caused by IAV infection. PPQ-B may down-regulate the NF-κB and MAPK pathways to inhibit both virus replication and inflammatory responses. In summary, PPQ-B has the potential to be developed into a novel anti-IAV drug targeting host EGFR pathway in the future.
Co-reporter:Lijuan Wu, Wei Wang, Xiaoshuang Zhang, Xia Zhao, Guangli Yu
Carbohydrate Polymers 2016 Volume 143() pp:139-148
Publication Date(Web):5 June 2016
DOI:10.1016/j.carbpol.2016.01.065
•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.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.
Co-reporter:Huquan Gao, Wenqiang Guo, Qiang Wang, Lianqing Zhang, Meilin Zhu, Tianjiao Zhu, Qianqun Gu, Wei Wang, Dehai Li
Bioorganic & Medicinal Chemistry Letters 2013 Volume 23(Issue 6) pp:1776-1778
Publication Date(Web):15 March 2013
DOI:10.1016/j.bmcl.2013.01.051
A new butenolide isoaspulvinone E (1), together with two known butenolides aspulvinone E (2) and pulvic acid (3) were isolated from the marine-derived fungus, Aspergillus terreus Gwq-48. They showed significant anti-influenza A H1N1 virus activities, with IC50 values of 32.3, 56.9, and 29.1 μg/mL, respectively. Moreover, only compound 1 exhibited effective inhibitory activity against H1N1 viral neuraminidase (NA), and docking of two isomers (1–2) into the active sites of NA showed that the E double bond Δ5(10) was essential to achieve activity.
Co-reporter:Wei Wang, Pan Zhang, Guang-Li Yu, Chun-Xia Li, Cui Hao, Xin Qi, Li-Juan Zhang, Hua-Shi Guan
Food Chemistry 2012 Volume 133(Issue 3) pp:880-888
Publication Date(Web):1 August 2012
DOI:10.1016/j.foodchem.2012.01.108
Carrageenans, the sulphated galactans derived from red algae, are attracting increasing interest in developing potential anti-viral drugs. In this study, low molecular weight κ-carrageenan oligosaccharides (KCO) and their sulphated derivatives (KCO-S) were prepared, and their anti-influenza A virus (IAV) properties were investigated. The results indicated that KCO and KCO-S could effectively inhibit IAV multiplication in MDCK cells in a dose-dependent manner. Furthermore, a structure–activity relationship study showed that the degree of sulphation and molecular weight were the main factors that influenced the anti-IAV activity of κ-carrageenan oligosaccharide. The most active κ-carrageenan oligosaccharide had a sulphate content of 0.8–1.0 mole/mole of disaccharide and a molecular weight of 1–3 kDa. In addition, KCO and KCO-S could significantly improve survival and decrease pulmonary viral titres in IAV-infected mice. Moreover, the antiviral effect of KCO and KCO-S does not seem to be dependent on the interferon system. In conclusion, carrageenan oligosaccharide and its sulphated derivative have good inhibitory actions on IAV replication in vitro and in vivo.Highlights► κ-Carrageenan oligosaccharide KCO and its sulphated derivative KCO-S were prepared. ► KCO and KCO-S could effectively inhibit IAV multiplication in vitro. ► KCO and KCO-S could improve survival and decrease viral titres in IAV-infected mice. ► The antiviral effect of KCO and KCO-S does not seem to be dependent on interferon.