Related Experiment Video

Updated: Aug 25, 2025

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

315

Mechanism of Gentisic Acid on Rheumatoid Arthritis Based on miR-19b-3p/RAF1 Axis

Dou Ding1, Qi Zhang1, Fu-Jia Zeng1

  • 1Department of Traditional Chinese Medicine, Zunyi Medical and Pharmaceutical College, Zunyi, Guizhou Province, 563006, China.

Chinese Journal of Integrative Medicine
|October 17, 2022
PubMed
Abstract

Insights

Gentisic acid (GA) treats rheumatoid arthritis (RA) by upregulating miR-19b-3p and downregulating RAF1, inhibiting cell growth and migration. This study reveals GA

Area of Science:

  • Molecular Biology
  • Immunology
  • Pharmacology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and destruction.
  • The miR-19b-3p/RAF1 axis plays a crucial role in the pathogenesis of RA.
  • Gentisic acid (GA) is being investigated for its potential therapeutic effects in RA.

Purpose of the Study:

  • To investigate the therapeutic effect of gentisic acid (GA) on rheumatoid arthritis (RA).
  • To elucidate the role of the miR-19b-3p/RAF1 axis in GA's therapeutic mechanism.
  • To determine GA's impact on cell proliferation, apoptosis, invasion, and migration in RA models.

Main Methods:

  • Cell counting kit-8 assay to determine GA's inhibitory concentration on MH7A cells.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) to measure miR-19b-3p and RAF1 expression.
  • Western blotting to assess RAF1, ERK1/2, and p-ERK1/2 levels.
  • Dual-luciferase assay, qRT-PCR, and Western blot to confirm miR-19b-3p targeting RAF1.
  • Flow cytometry, Transwell, and wound healing assays to evaluate apoptosis, invasion, and migration.

Main Results:

  • Gentisic acid (GA) demonstrated dose-dependent inhibition of MH7A cell growth, with a calculated IC50 of 67.019 mmol/L.
  • GA treatment upregulated miR-19b-3p, downregulated RAF1, inhibited ERK1/2 phosphorylation, induced apoptosis, and suppressed invasion and migration of MH7A cells.
  • RAF1 was confirmed as a direct target of miR-19b-3p, and its inhibition reversed the effects of miR-19b-3p upregulation.
  • Inhibition of miR-19b-3p led to increased RAF1 expression, ERK1/2 phosphorylation, cell invasion, and migration, while suppressing apoptosis.

Conclusions:

  • Gentisic acid (GA) exerts therapeutic effects on rheumatoid arthritis (RA) by modulating the miR-19b-3p/RAF1 axis.
  • The miR-19b-3p/RAF1 axis mediates the ERK signaling pathway, influencing RA development.
  • GA's regulation of this axis inhibits RA progression by affecting cell apoptosis, invasion, and migration.
Keywords:
MAPK/ERKRAF1gentisic acidmiR-19b-3prheumatoid arthritis

More Related Videos

Preliminary Study on Acupuncture Combined with Grain-sized Moxibustion for Treating Rheumatoid Arthritis with Finger Joint Pain04:50

Preliminary Study on Acupuncture Combined with Grain-sized Moxibustion for Treating Rheumatoid Arthritis with Finger Joint Pain

Published on: May 16, 2025

314
An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

7.3K

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.1K
Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
14.0K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.6K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
4.1K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.9K
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
31