Article Sidebar
Published:
Oct 8, 2023Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Effect of entecavir on IL-6/STAT3/SOCS3 pathway in patients with chronic hepatitis B-induced liver fibrosis
Abstract
Purpose: To evaluate the impact of entecavir (ENT) on patients with liver fibrosis resulting from chronic hepatitis B (CHB) and its association with the interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3)/suppressor of cytokine signaling 3 (SOCS3) pathway.
Methods: Thirty-one patients with liver fibrosis received ENT at a dose of 0.5 mg/day for 48 weeks. Relevant protein levels in patient’s serum before and after treatment were assayed using enzyme-linked immunosorbent assay (ELISA). Furthermore, human hepatic stellate cells (HSCs) were cultured in vitro and divided into three groups: control, transforming growth factor beta 1 (TGF-β1) induction (TGF-β1 group), and ENT treatment (TGF-β1 + ENT group). Protein levels in the supernatant were assayed using ELISA, while the expression levels of related genes were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Expression of α-SMA was visualized using immunofluorescence assay and the relevant protein levels were determined by Western blotting.
Results: Treatment with ENT significantly decreased (p < 0.01) IL-6 and STAT3 expression, increased SOCS3 expression and significantly reduced (p < 0.01) the concentrations of hyaluronic acid (HA), type IV collagen (IVC), laminin (LN) and pro-collagen type III (PCIII) in patients with liver fibrosis. TGF-β1 significantly (p < 0.01) elevated IL-6, STAT3 and Col-I expressions and a tissue inhibitor of metalloproteinases-1 (TIMP-1) suppressed the expression of SOCS3 in human HSCs and induced fibrosis. Entecavir mitigated TGF-β1-induced fibrogenesis in HSCs (p < 0.01).
Conclusion: Entecavir has a positive effect on liver fibrosis resulting from CHB by regulating IL- 6/STAT3/SOCS3 pathway. Future research will focus on conducting larger clinical trials to further validate these findings and explore the long-term effects of ENT on liver fibrosis progression and patient outcomes.
