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Home > Archive > Herpes support > November 2005 > Limonium sinense
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| Perl Molson 2005-11-19, 12:54 pm |
| Samarangenin B from Limonium sinense Suppresses Herpes Simplex Virus
Type 1 Replication in Vero Cells by Regulation of Viral Macromolecular
Synthesis
Yuh-Chi Kuo,1,2* Lie-Chwen Lin,1 Wei-Jern Tsai,1 Cheng-Jen Chou,1
Szu-Hao Kung,3 and Yen-Hui Ho1
National Research Institute of Chinese Medicine,1 Institute of Life
Science, Fu-Jen University,2 Department of Medical Technology and
Institute of Biotechnology in Medicine, National Yang-Ming University,
Taipei, Taiwan3
Received 30 November 2001/ Returned for modification 12 March 2002/
Accepted 30 May 2002
Inhibitory effects of ethanolic extracts from 10 Chinese herbs on
herpes simplex virus type 1 (HSV-1) replication were investigated. By a
bioassay-guided fractionation procedure, samarangenin B (Sam B) was
isolated from Limonium sinense; Sam B significantly suppressed HSV-1
multiplication in Vero cells without apparent cytotoxicity.
Time-of-addition experiments suggested that the inhibitory action of
Sam B on HSV-1 replication was not due to the blocking of virus
adsorption. In an attempt to further localize the point in the HSV-1
replication cycle where arrest occurred, a set of key regulatory events
leading to viral multiplication was examined, including viral
immediate-early (), early (=DF), and late () gene expression and DNA
replication. Results indicated that levels of glycoprotein B (gB), gC,
gD, gG, and infected-cell protein 5 (ICP5) expression and gB mRNA
expression in Vero cells were impeded by Sam B. Data from PCR showed
that replication of HSV-1 DNA in Vero cells was arrested by Sam B.
Furthermore, Sam B decreased DNA polymerase, ICP0, and ICP4 gene
expression in Vero cells. Results of an electrophoretic mobility shift
assay demonstrated that Sam B interrupted the formation of an
-trans-induction factor/C1/Oct-1/GARAT multiprotein complex. The
mechanisms of antiviral action of Sam B seem to be mediated, at least
in part, by inhibiting HSV-1 gene expression, including expression of
the ICP0 and ICP4 genes, by blocking =DF transcripts such as DNA
polymerase mRNA, and by arresting HSV-1 DNA synthesis and structural
protein expression in Vero cells. These results show that Sam B is an
antiviral agent against HSV-1 replication.
http://aac.asm.org/cgi/content/abstract/46/9/2854
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| Perl Molson 2005-11-19, 12:54 pm |
| http://ghs.gresham.k12.or.us/scienc.../parsley/pars.=
htm
Aparrently, this plant is Alpine Lovage (root)
Perl Molson wrote:
> Samarangenin B from Limonium sinense Suppresses Herpes Simplex Virus
> Type 1 Replication in Vero Cells by Regulation of Viral Macromolecular
> Synthesis
> Yuh-Chi Kuo,1,2* Lie-Chwen Lin,1 Wei-Jern Tsai,1 Cheng-Jen Chou,1
> Szu-Hao Kung,3 and Yen-Hui Ho1
> National Research Institute of Chinese Medicine,1 Institute of Life
> Science, Fu-Jen University,2 Department of Medical Technology and
> Institute of Biotechnology in Medicine, National Yang-Ming University,
> Taipei, Taiwan3
>
> Received 30 November 2001/ Returned for modification 12 March 2002/
> Accepted 30 May 2002
>
> Inhibitory effects of ethanolic extracts from 10 Chinese herbs on
> herpes simplex virus type 1 (HSV-1) replication were investigated. By a
> bioassay-guided fractionation procedure, samarangenin B (Sam B) was
> isolated from Limonium sinense; Sam B significantly suppressed HSV-1
> multiplication in Vero cells without apparent cytotoxicity.
> Time-of-addition experiments suggested that the inhibitory action of
> Sam B on HSV-1 replication was not due to the blocking of virus
> adsorption. In an attempt to further localize the point in the HSV-1
> replication cycle where arrest occurred, a set of key regulatory events
> leading to viral multiplication was examined, including viral
> immediate-early (), early (=DF), and late () gene expression and DNA
> replication. Results indicated that levels of glycoprotein B (gB), gC,
> gD, gG, and infected-cell protein 5 (ICP5) expression and gB mRNA
> expression in Vero cells were impeded by Sam B. Data from PCR showed
> that replication of HSV-1 DNA in Vero cells was arrested by Sam B.
> Furthermore, Sam B decreased DNA polymerase, ICP0, and ICP4 gene
> expression in Vero cells. Results of an electrophoretic mobility shift
> assay demonstrated that Sam B interrupted the formation of an
> -trans-induction factor/C1/Oct-1/GARAT multiprotein complex. The
> mechanisms of antiviral action of Sam B seem to be mediated, at least
> in part, by inhibiting HSV-1 gene expression, including expression of
> the ICP0 and ICP4 genes, by blocking =DF transcripts such as DNA
> polymerase mRNA, and by arresting HSV-1 DNA synthesis and structural
> protein expression in Vero cells. These results show that Sam B is an
> antiviral agent against HSV-1 replication.
>=20
> http://aac.asm.org/cgi/content/abstract/46/9/2854
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