Oxymatrine Inhibition of Hepatitis B Virus Replication Through ERK1/2 Pathway and HNF1α and HNF4α Block in vitro.
J Coll Physicians Surg Pak
; 34(3): 329-335, 2024 Mar.
Article
en En
| MEDLINE
| ID: mdl-38462870
ABSTRACT
OBJECTIVE:
To explore the molecular mechanism of oxymatrine (OM) by increasing the phosphorylation of ERK1/2 signal factor and blocking the transcription factors HNF1α and HNF4α expression against hepatitis B virus (HBV) antigen secretion and HBV DNA replication in HepG2.2.15 cells. STUDYDESIGN:
An experimental study. Place and Duration of the Study Department of Laboratory Medicine, First Affiliated Hospital of Gannan Medical University, Jiangxi, China, between May 2020 and December 2022.METHODOLOGY:
HepG2.2.15 cells, known for stably expressing HBV particles, were utilised as a cell-based model to explore potential pathways pertaining to the OM inhibition of HBV replication. An MTT assay was utilised to measure cytotoxicity. HBsAg or HBeAg content was measured using an enzyme-linked immunosorbent assay kit. HBV DNA in cell-free culture media was examined using a fluorescent quantitative PCR kit. Real-time PCR was utilised to analyse HNF1α and HNF4α mRNA expression, whereas Western blotting was performed to evaluate HNF1α, HNF4α, and ERK1/2 protein expression.RESULTS:
OM inhibited HBV DNA copy number in the cell supernatant, 3.5-kb RNA gene expression in cells, and HBsAg and HBeAg secretion. OM upregulated p-ERK1/2 protein and significantly downregulated HNF1α and HNF4α gene transcription and protein translation.CONCLUSION:
OM may inhibit the replication of HBV by inducing the phosphorylation of ERK1/2 and blocking the transcription factors HNF1α and HNF4α expression that are essential for viral replication. KEY WORDS Oxymatrine, ERK1/2, Hepatocyte nuclear factor, Anti-HBV.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Virus de la Hepatitis B
/
Matrinas
/
Hepatitis B
Límite:
Humans
Idioma:
En
Revista:
J Coll Physicians Surg Pak
Asunto de la revista:
MEDICINA
Año:
2024
Tipo del documento:
Article
País de afiliación:
China