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Attenuation of Influenza Virus Infectivity with Herbal-Marine Compound (HESA-A): an in vitro Study in MDCK Cells

tetano

Editor, Senior Moderator
Virol J. 2012 Feb 16;9(1):44. [Epub ahead of print]
Attenuation of Influenza Virus Infectivity with Herbal-Marine Compound (HESA-A): an in vitro Study in MDCK Cells.
Mehrbod P, Ideris A, Omar AR, Hair-Bejo M, Sheau Wei T, Kheiri MT, Tabatabaian M.
Abstract

ABSTRACT:
BACKGROUND:

The influenza virus is still one of the most important respiratory risks affecting humans which require effective treatments. In this case, traditional medications are of interest. HESA-A is an active natural biological compound from herbal-marine origin. Previous studies have reported that the therapeutic properties of HESA-A are able to treat psoriasis vulgaris and cancers. However, no antiviral properties have been reported.
METHODS:

This study was designed to investigate the potential antiviral properties of HESA-A and its effects in modulating TNF-alpha and IL-6 cytokine levels. HESA-A was prepared in normal saline as a stock solution (0.8 mg/ml, pH = 7.4). Percentages of cell survival when exposed to different concentrations of HESA-A at different time intervals was determined by MTT assay. To study the potential antiviral activity of HESA-A, Madin-Darby Canine Kidney (MDCK) cells were treated with the effective concentration (EC50) of HESA-A (0.025 mg/ml) and 100 TCID50/0.1 ml of virus sample under different types of exposure.
RESULTS:

Based on the MTT method and hemagglutination assay (HA), HESA-A is capable of improving cell viability to 31% and decreasing HA titre to almost 99% in co-penetration exposures. In addition, based on quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), it was found that HESA-A causes decrements in TNF-alpha and IL-6 cytokine expressions, which was significant for TNF-alpha (p [less than or equal to] 0.05) but not for IL-6 .
CONCLUSION:

In conclusion, HESA-A was effective against influenza infection through suppressing cytokine expression.

PMID:
22340010
[PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/22340010
 
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