Related Experiment Video
Updated: Apr 6, 2026

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
Apoptotic Effect of Geniposide on Fibroblast-Like Synoviocytes in Rats with Adjuvant-Induced Arthritis via Inhibiting
Rong Li1, Li Cai2, Wen-Jian Tang1
1School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei, China.
Abstract:
Stimulating fibroblast-like synoviocyte (FLS) apoptosis in rheumatoid arthritis (RA) is a promising strategy for clinical treatment. Previous studies have confirmed that geniposide shows a certain anti-arthritic effect in vivo. However, whether geniposide can induce RA FLS apoptosis and the underlying mechanisms has not been elucidated. Herein, adjuvant-induced arthritis (AIA) in rat was induced and FLS was isolated from synovial tissues by tissue explant cultivation method. MTT assay, Hoechst staining, and flow cytometric apoptosis assay were applied to evaluate apoptotic effect of geniposide on AIA FLS. Bcl-2, Bax, and caspase 3 messenger RNA (mRNA) levels, and extracellular-signal-regulated kinases (ERKs) and phosphorylated ERK protein levels were examined by real-time PCR and western blot, respectively. We found that geniposide dose-dependently inhibited AIA FLS proliferation in vitro. AIA FLS treated with geniposide displayed typical apoptotic morphological characteristics including nuclear shrinkage and chromatin condensation. Flow cytometric apoptosis assay indicated that geniposide significantly increased the apoptosis rate of AIA FLS. Additionally, geniposide treatment on AIA FLS decreased Bcl-2 mRNA level and increased Bax and caspase 3 mRNA levels, accompanied by reduced protein levels of phosphorylated-ERK1/2, without affecting total ERK1/2. In conclusion, geniposide effectively induces AIA FLS apoptosis through regulating the apoptosis-related gene expressions and inhibiting ERK signal pathway.
Insights
Geniposide effectively induces apoptosis in fibroblast-like synoviocytes (FLS) from rats with rheumatoid arthritis. This compound regulates apoptosis-related gene expression and inhibits the ERK signaling pathway, offering a potential therapeutic strategy.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Rheumatoid arthritis (RA) involves fibroblast-like synoviocyte (FLS) proliferation.
- Geniposide has demonstrated in vivo anti-arthritic effects.
- Mechanisms of geniposide's action on RA FLS apoptosis remain unclear.
Purpose of the Study:
- To investigate geniposide's ability to induce apoptosis in adjuvant-induced arthritis (AIA) rat FLS.
- To elucidate the underlying molecular mechanisms of geniposide-induced apoptosis in AIA FLS.
Main Methods:
- Adjuvant-induced arthritis (AIA) rat model established, FLS isolated via tissue explant.
- MTT assay, Hoechst staining, and flow cytometry assessed apoptosis.
- Real-time PCR and Western blot analyzed gene and protein expression (Bcl-2, Bax, caspase 3, ERK/p-ERK).
Main Results:
- Geniposide dose-dependently inhibited AIA FLS proliferation in vitro.
- Geniposide induced morphological apoptotic changes and significantly increased AIA FLS apoptosis rate.
- Geniposide altered apoptosis-related gene expression (decreased Bcl-2, increased Bax, caspase 3) and inhibited ERK signaling pathway (reduced p-ERK1/2).
Conclusions:
- Geniposide effectively induces apoptosis in AIA rat FLS.
- Geniposide exerts its effects by modulating apoptosis-related gene expression and inhibiting the ERK signaling pathway.
- Geniposide represents a potential therapeutic agent for rheumatoid arthritis by targeting FLS apoptosis.
Related Concept Videos
The JAK-STAT Signaling Pathway
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
