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Osthole Improves Rat Arthritis Through the miR-34a/Bcl-2 Axis
Honghua Yuan1, Jun Yi2, Enhu Bao2
1Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, and Public Experimental Research Center, Xuzhou Medical University.
Journal of Visualized Experiments : Jove
|June 1, 2026
Summary
Osthole (OST) protects knee joint cartilage cells from damage and inflammation in osteoarthritis models. It works by promoting cell repair processes and reducing cell death through the miR-34a/Bcl-2 pathway, offering potential for new KOA treatments.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Knee osteoarthritis (KOA) is a widespread degenerative joint disease with limited treatment options.
- Current KOA therapies have drawbacks including side effects, low efficacy, and invasiveness.
Purpose of the Study:
- To investigate the protective effects and underlying mechanisms of Osthole (OST) on chondrocytes in knee osteoarthritis models.
- To evaluate OST's potential as a therapeutic agent for KOA.
Main Methods:
- In vitro and in vivo studies using CCK8 assay, transmission electron microscopy (TEM), H&E staining, and serum biochemical analysis.
- Analysis of autophagy and apoptosis via TEM, acridine orange staining, flow cytometry, and western blotting.
- Mechanistic investigation using qRT-PCR and luciferase reporter assays to explore the miR-34a/Bcl-2 pathway.
Main Results:
- OST demonstrated protective effects on chondrocytes in vitro and in vivo without significant toxicity.
- OST promoted chondrocyte autophagy and suppressed apoptosis.
- OST downregulated miR-34a, leading to increased Bcl-2 expression and inhibition of apoptosis via the miR-34a/Bcl-2 pathway.
- OST attenuated LPS-induced stress, inflammation, and apoptosis in a rat model of KOA.
Conclusions:
- Osthole exhibits significant chondroprotective effects in knee osteoarthritis by modulating autophagy and apoptosis.
- The therapeutic mechanism involves the downregulation of miR-34a and subsequent upregulation of Bcl-2.
- These findings support OST's potential for developing novel therapeutic strategies and patented drugs for KOA treatment.