IMR Press / FBE / Volume 2 / Issue 4 / DOI: 10.2741/E213

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Scutellariae radix suppresses hepatitis B virus production in human hepatoma cells

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1 Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan, R.O.C.
2 Graduate Institute of Natural Product, Chang Gung University, Tao-Yuan, Taiwan, R.O.C.
3 Department of Life Science, Chang Gung University, Tao-Yuan, Taiwan, R.O.C.
Academic Editor:Lo Szecheng
Front. Biosci. (Elite Ed) 2010, 2(4), 1538–1547; https://doi.org/10.2741/E213
Published: 1 June 2010
(This article belongs to the Special Issue Molecular biology and pathogenesis of HBV and HDV)
Abstract

The traditional Chinese medicine Xiao-Chai-Hu-Tang (HD-7) has been widely used to treat liver diseases in China and Japan. HD-7 consists of seven different ingredients, but which one provides the therapeutic benefits is still unknown. Here, we identified the "Minister herb" Scutellariae radix (HD-1S), but not the "King herb" Bupleuri radix (HD-1B) in HD-7, as the active component that suppresses HBV gene expression and virus production in human hepatoma cells. We have found that an aqueous extract of HD-1S not only suppressed wild-type virus but also lamivudine-resistant HBV mutant in human hepatoma cells. We show that HD-1S selectively suppresses HBV core promoter activity. Electrophoretic mobility shift assay analysis has revealed that HD-1S treatment decreases the DNA-binding activity of nuclear extract of HepA2 cells to a specific cis-element of the HBV core promoter, which includes the peroxisome proliferator-activated receptor binding site and HNF4. Furthermore, ectopic expression of PGC-1 abolished the suppression of HD-1S on HBV core promoter activity suggesting that HD-1S may act through modulating hepatic transcriptional machinery to suppress HBV viral gene expression and virus production.

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