Hepatitis B virus replication causes oxidative stress in HepAD38 liver cells

Severi, Tamara; Ying, Chunxiao; Vermeesch, Joris Robert; Cassiman, David; Cnops, Lieselotte; Verslype, Chris; Fevery, Johan; Arckens, Lutgarde; Neyts, Johan; Pelt, Jos van

doi:10.1007/s11010-006-9167-x

Cited by 58 publications

(52 citation statements)

References 24 publications

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“…Valgimigli et al reported that ROS levels in HBV chronic hepatitis patients were higher than in healthy controls by radical probe electron paramagnetic resonance measurements of human liver biopsy specimens (41). In addition, induction of HBV replication in human hepatoma HepAD38 cells, in which HBV production is under the control of a tetracycline-regulated promoter, led to up-regulation of genes related to oxidative stress (42). The fact that the liver histopathology (Fig.…”

Section: Discussionmentioning

confidence: 95%

Chemopreventive Effect of Silymarin on Liver Pathology in HBV X Protein Transgenic Mice

Kao

et al. 2008

Cancer Research

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There are currently limited therapeutic regimens available for effective treatment of hepatocellular carcinoma (HCC). Silymarin is a naturally derived polyphenolic antioxidant with hepatoprotective properties and is very widely used in clinical application; however, effect of silymarin on spontaneous HCC has not been studied. Silymarin was evaluated for its efficacy against spontaneous carcinogenesis using the HBV X protein (HBx) transgenic model. Silymarin was p.o. given to the HBx transgenic mice from 4 to 6 weeks of age. Our data indicated that silymarin has therapeutic effects on the early stages of liver damage, reversing fatty changes and recovering liver histopathology in a dose-dependent manner. To study the chemopreventive effects on the later stages of carcinogenesis, the mice at 13 months were split into a precancerous group and a group with significant liver carcinogenesis. After silymarin was given to the precancerous mice from 13 to 16 months of age, in contrast to an 80% incidence of HCC development in the untreated transgenic mice, no HCC was detected in any of these mice. Nonetheless, small hyperplastic nodules were detected in 86% of these precancerous mice. In the second group with notable HCC, silymarin was unable to block cancer progression. Although silymarin did not affect HBx expression, intracellular reactive oxygen species levels were decreased, cell proliferation was stimulated, and hepatocyte ultrastructure was found to significantly recover. In conclusion, silymarin exerts beneficial effects on the early stages of liver pathogenesis, preventing and delaying liver carcinogenesis. This drug should be considered as a potential chemopreventive agent for HBV-related hepatocarcinogenesis.

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Section: Discussionmentioning

confidence: 95%

Chemopreventive Effect of Silymarin on Liver Pathology in HBV X Protein Transgenic Mice

Kao

et al. 2008

Cancer Research

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“…1). There have been many studies on oxidative stress production by HBV using HBV-Tg mice or HBV DNA transfection [1,33]. Reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, as well as hydroxyl radical may damage cellular macromolecules [34].…”

Section: Discussionmentioning

confidence: 99%

Expression of hepatitis B virus proteins in transgenic mice alters lipid metabolism and induces oxidative stress in the liver

Yang¹,

Yan²,

He³

et al. 2008

Journal of Hepatology

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“…Based on the previous study that HBVinduced ROS can cause HCC [3,4,14] and the expression level of Hsp90 is elevated in HCC tumor tissue [15], we hypothesized that ROS might improve Hsp90-driven HBV production. In this research, we exploited cell-free system and HepG2.2.15 cells to test the functional significance of ROS in Hsp90-driven HBV capsid formation.…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species promote heat shock protein 90-mediated HBV capsid assembly

Kim

Seo

Jung

2015

Biochemical and Biophysical Research Communications

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Hepatitis B virus replication causes oxidative stress in HepAD38 liver cells

Abstract: HBV replication modulates host gene expression and induces oxidative stress. In this HepAD38 model early events (0-4 days) in the host cell after induction of HBV replication can be studied under strictly defined conditions.

Cited by 58 publications

References 24 publications

Chemopreventive Effect of Silymarin on Liver Pathology in HBV X Protein Transgenic Mice

Chemopreventive Effect of Silymarin on Liver Pathology in HBV X Protein Transgenic Mice

Expression of hepatitis B virus proteins in transgenic mice alters lipid metabolism and induces oxidative stress in the liver

Reactive oxygen species promote heat shock protein 90-mediated HBV capsid assembly

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