Panduratin A from Boesenbergia rotunda suppresses hepatitis B virus by targeting HNF1α and synergizing with antiviral agents
4
Issued Date
2026-12-01
Resource Type
ISSN
19910150
eISSN
17498546
Scopus ID
2-s2.0-105026893143
Journal Title
Chinese Medicine United Kingdom
Volume
21
Issue
1
Rights Holder(s)
SCOPUS
Bibliographic Citation
Chinese Medicine United Kingdom Vol.21 No.1 (2026)
Suggested Citation
Thongsri P., Pewkliang Y., Borwornpinyo S., Wongkajornsilp A., Ruenraroengsak P., Anurathapan U., Sobhonslidsuk A., Hongeng S., Sa-ngiamsuntorn K. Panduratin A from Boesenbergia rotunda suppresses hepatitis B virus by targeting HNF1α and synergizing with antiviral agents. Chinese Medicine United Kingdom Vol.21 No.1 (2026). doi:10.1186/s13020-025-01285-w Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/114407
Title
Panduratin A from Boesenbergia rotunda suppresses hepatitis B virus by targeting HNF1α and synergizing with antiviral agents
Corresponding Author(s)
Other Contributor(s)
Abstract
Background: Boesenbergia rotunda (fingerroot) is widely used in traditional medicine, and its bioactive compound panduratin A has demonstrated potent antiviral properties. However, the mechanistic basis underlying its anti-hepatitis B virus (HBV) activity remains to be fully elucidated. Methods: HBV-infected human hepatocytes (imHCs) were treated with B. rotunda extract, panduratin A, or pinostrobin. Intracellular HBV DNA, secreted HBsAg and HBeAg, and pregenomic RNA (pgRNA) were quantified in dose- and time-dependent experiments. Luciferase reporter assays were used to assess HBV promoter activity. The roles of HNF1α and HNF4α were evaluated by siRNA-mediated knockdown and ectopic gene expression. Drug interaction studies were performed using the KDM5 inhibitor GS-5801 and the capsid assembly modulator NVR-3778. A 3D liver spheroid model was used to validate antiviral effects on HBV DNA and cccDNA. Gene interaction network analysis was conducted to identify central regulatory pathways. Results: B. rotunda extract, panduratin A, and pinostrobin significantly suppressed intracellular HBV DNA, HBsAg, HBeAg, and pgRNA. Panduratin A exhibited the strongest antiviral activity and inhibited preS1, preS2, and core promoter activities. Panduratin A markedly downregulated HNF1α expression, with only modest effects on HNF4α. Knockdown of HNF1α significantly reduced the antiviral efficacy of panduratin A, whereas ectopic HNF1α expression rescued its inhibitory effects. Co-treatment with GS-5801 produced synergistic activity, and combination with NVR-3778 yielded additive antiviral effects. In 3D liver spheroids, panduratin A reduced intracellular HBV DNA and cccDNA with minimal cytotoxicity. Network analysis further identified HNF1α as a key regulatory node modulated by panduratin A. Conclusion: Panduratin A is a potent anti-HBV compound that acts primarily through HNF1α-dependent suppression of HBV transcription and replication. Its efficacy in combination therapy and in 3D liver models highlights its potential as a promising candidate for future HBV treatment strategies.