The traditional Chinese medicine Oenanthe javanica (OJ) has been used for many years, mainly for the treatment of inflammatory conditions including hepatitis. In this study, human hepatoma Hep G2.2.15 cells culture system and duck hepatitis B virus (DHBV) infection model were used as in vivo and in vitro models to evaluate the anti-HBV effects of total phenolics from Oenanthe javanica (OJTP). The HBeAg and HBsAg concentrations in cell culture medium were determined by using the enzyme immunoassay kit after Hep G2.2.15 cells were treated with OJTP for 9 d. DHBV-DNA in duck serum was analyzed by dot blot hybridization assay. In the cell model, OJTP could dose-dependently inhibit the production of the HBeAg and HBsAg, and the inhibition rates of OJTP on HBeAg and HBsAg in the Hep G2.2.15 cells were 70.12% and 72.61% on day 9, respectively. In the DHBV infection model, OJTP also reduced HBV DNA level in a dose-dependent manner. The DHBV-DNA levels decreased significantly after the treatment with 0.10 g kg(-1)d(-1) and 0.20 g kg(-1)d(-1) OJTP. The inhibition of the peak of viremia was at the maximum at the dose of 0.20 g kg(-1)d(-1) and reached 64.10% on day 5 and 66.48% on day 10, respectively. Histopathological evaluation of the liver revealed significant improvement by OJTP. In conclusion, our results demonstrate that OJTP can efficiently inhibit HBV replication in Hep G2.2.15 cells line in vitro and inhibit DHBV replication in ducks in vivo. OJTP therefore warrants further investigation as a potential therapeutic agent for HBV infections.
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http://dx.doi.org/10.1016/j.jep.2008.03.024 | DOI Listing |
Mutat Res
September 2000
Department of Pathology and Laboratory Medicine, MCP and Hahnemann School of Medicine, MCP Hahnemann University, Broad and Vine, Philadelphia, PA 19102-1192, USA.
Hepatitis B virus (HBV) is a major etiological factor associated with hepatocarcinogenesis, but its role in the transformation process remains unclear. We previously documented the accumulation of genetic alterations in a HBV-transfected cell line. In the present study, we addressed the effect of HBV and its replication on the genome and phenotype of the host cell.
View Article and Find Full Text PDFCancer Genet Cytogenet
January 2000
MCP Hahnemann University, School of Medicine, Department of Pathology, Philadelphia, Pennsylvania, USA.
Recent data suggest that Bin1, a novel C-MYC interacting protein, is a suppressor gene whose loss of expression is a frequent aberration associated with several malignancies. The mechanism responsible for loss of BIN1 expression is not understood. The purpose of this study is to investigate DNA profile of the BIN1 gene in human hepatoma Hep G2 cells, previously documented with lack of BIN1 expression.
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