Inhibition of H1N1 influenza A virus growth and induction of inflammatory mediators by the isoquinoline alkaloid berberine and extracts of goldenseal (Hydrastis canadensis)

Cecil, Chad; Davis, Jeanine M.; Cech, Nadja B.; Laster, Scott M.

doi:10.1016/j.intimp.2011.06.002

Cited by 74 publications

(48 citation statements)

References 68 publications

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“…Berberine (BBR), an isoquinoline alkaloid isolated from traditional medicine herbs including Rhizoma coptidis and Cortex phellodendri has exhibited significant anti-viral efficacy against various viruses including influenza virus, HIV, human cytomegalovirus, and herpes simplex virus (HSV) [10–13]. It has been shown that BBR can inhibit virus infection by directly affecting individual steps of the virus replication cycle [13], inhibiting viral protein translocation, or by regulating host signal pathways [10].…”

Section: Introductionmentioning

confidence: 99%

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Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro

Dai

Zhang

et al. 2017

Med Sci Monit

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BackgroundAt present, the treatment of coxsackievirus-induced myocarditis remains difficult. Berberine (BBR), an isoquinoline alkaloid isolated from traditional medicine herbs, exhibits significant anti-viral efficacy against various viruses. However, the underlying mechanism by which BBR controls CVB3 infection has not yet been reported. The purpose of this study was to investigate the anti-viral efficacy of BBR against CVB3 infection and its mechanism.Material/MethodsIn our experiments, the protein levels of VP1 and MAPKs signal pathway were measured by Western blot. The mRNA level of VP1 was measured by RT-PCR. The virus titers were determined by TCID50 assay.ResultsWe found that BBR treatment significantly decreased CVB3 replication in HeLa cells. In addition, the BBR treatment reduced the phosphorylation levels of JNK and p38 MAPK upon CVB3 infection in both HeLa cells and primary rat myocardial cells.ConclusionsTaken together, these results suggest that BBR inhibits CVB3 replication through the suppression of JNK and p38 MAPK activation, shedding new light on the investigation of therapeutic strategies against CVB3-induced viral myocarditis.

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Section: Introductionmentioning

confidence: 99%

“…It has been shown that BBR can inhibit virus infection by directly affecting individual steps of the virus replication cycle [13], inhibiting viral protein translocation, or by regulating host signal pathways [10]. …”

Section: Introductionmentioning

confidence: 99%

Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro

Dai

Zhang

et al. 2017

Med Sci Monit

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“…Over the past several decades, numerous biological effects of berberine have been discovered, such as its anticancer [6], antilipogenic and hypoglycemic [7], neuroprotective [8], and antimicrobial effects against fungal pathogens [9] and bacterial pathogens [10]. In addition, berberine has been shown to exert antiviral effects against viruses such as herpes simplex virus, human cytomegalovirus, and influenza A virus [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of respiratory syncytial virus replication and virus-induced p38 kinase activity by berberine

Shin

Choi

et al. 2015

International Immunopharmacology

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“…Berberine exhibits inhibitory activity against some viruses, including influenza A virus (39) and human cytomegalovirus (40). Chin et al first reported that berberine from Coptidis rhizoma showed an anti-HSV effect (41).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Cellular c-Jun N-Terminal Protein Kinase and NF-κB Activation by Berberine May Result in Inhibition of Herpes Simplex Virus Replication

Song

Qiu

Chu

et al. 2014

Antimicrob Agents Chemother

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bBerberine is a quaternary ammonium salt from the protoberberine group of isoquinoline alkaloids. Some reports show that berberine exhibits anti-inflammatory, antitumor, and antiviral properties by modulating multiple cellular signaling pathways, including p53, nuclear factor B (NF-B), and mitogen-activated protein kinase. In the present study, we investigated the antiviral effect of berberine against herpes simplex virus (HSV) infection. Current antiherpes medicines such as acyclovir can lessen the recurring activation when used early at infection but are unable to prevent or cure infections where treatment has selected for resistant mutants. In searching for new antiviral agents against herpesvirus infection, we found that berberine reduced viral RNA transcription, protein synthesis, and virus titers in a dose-dependent manner. To elucidate the mechanism of its antiviral activity, the effect of berberine on the individual steps of viral replication cycle of HSV was investigated via time-of-drug addition assay. We found that berberine acted at the early stage of HSV replication cycle, between viral attachment/entry and genomic DNA replication, probably at the immediate-early gene expression stage. We further demonstrated that berberine significantly reduced HSV-induced NF-B activation, as well as IB-␣ degradation and p65 nuclear translocation. Moreover, we found that berberine also depressed HSV-induced c-Jun N-terminal kinase (JNK) phosphorylation but had little effect on p38 phosphorylation. Our results suggest that the berberine inhibition of HSV infection may be mediated through modulating cellular JNK and NF-B pathways.

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Inhibition of H1N1 influenza A virus growth and induction of inflammatory mediators by the isoquinoline alkaloid berberine and extracts of goldenseal (Hydrastis canadensis)

Cited by 74 publications

References 68 publications

Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro

Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro

Inhibition of respiratory syncytial virus replication and virus-induced p38 kinase activity by berberine

Downregulation of Cellular c-Jun N-Terminal Protein Kinase and NF-κB Activation by Berberine May Result in Inhibition of Herpes Simplex Virus Replication

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