Related Experiment Video
Updated: May 21, 2026
09:02
Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
Wedelolactone Inhibits Hepatitis B Virus Replication by Modulating NF-κB and Nrf2/HO-1 Signaling: An in-vitro Huh7
Bin Wang1, Xuehui Bu1, Umar Saeed2,3
1Department of Hepatology, Public Health Clinical Center Affilliated to Shandong University, Jinan, China.
Iranian Journal of Pharmaceutical Research : IJPR
|May 20, 2026
Summary
Wedelolactone shows promise for treating chronic hepatitis B (HBV) infection by reducing viral replication and liver damage. This compound offers combined antiviral and hepatoprotective effects, addressing limitations of current HBV therapies.
Area of Science:
- Hepatology
- Virology
- Pharmacology
Background:
- Chronic hepatitis B virus (HBV) infection causes liver injury via viral replication, inflammation, and oxidative stress.
- Current antiviral drugs inadequately address viral transcription and liver injury, highlighting the need for agents with combined antiviral and hepatoprotective properties.
Purpose of the Study:
- To investigate the effects of wedelolactone on HBV replication, gene expression, inflammation, and oxidative stress in an in vitro HBV model.
- To assess wedelolactone's potential as a dual-action therapeutic for chronic hepatitis B.
Main Methods:
- Human hepatocellular carcinoma cells (Huh7) were transfected with an HBV plasmid and treated with varying concentrations of wedelolactone.
- Assays included luciferase for promoter activity, blotting for transcripts and viral antigens (HBx), qPCR for HBV DNA, and Western blotting for inflammatory and oxidative stress markers (NF-κB, Nrf2, HO-1).
Main Results:
- Wedelolactone significantly suppressed HBV promoter activity, RNA transcription, core particle formation, and extracellular HBV DNA.
- The compound reduced viral antigen expression (HBcAg, HBsAg), inhibited NF-κB activation and inflammatory cytokine release.
- Wedelolactone enhanced Nrf2/HO-1 antioxidant signaling by reducing Keap1 levels, promoting heme oxygenase-1 induction.
Conclusions:
- Wedelolactone demonstrates dual antiviral and hepatoprotective effects against HBV infection.
- Its mechanism involves inhibiting HBV replication and modulating inflammatory and oxidative stress pathways, offering a potential new therapeutic strategy.
Keywords:
Antiviral ActivityHBV ReplicationHepatitis B VirusInflammationNF-κB SignalingNrf2/HO-1 Pathway.Oxidative StressWedelolactoneMore Related Videos
Related Concept Videos
01:25Hepatitis
Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
01:28Viral Hepatitis I: Introduction
Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
01:30Inhibitors of Viral Protein Synthesis
Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
01:29Viruses with RNA Genomes
RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
02:26NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
01:17Hepatic Drug Excretion: Enterohepatic Cycling
Enterohepatic cycling involves the active secretion of drugs and their metabolites into the bile via transporters in the canalicular membrane of hepatocytes. This secretion is an integral part of the digestive process, releasing these substances into the gastrointestinal (GI) tract.
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...