Propionate attenuates osteoarthritis progression by regulating the gut-joint axis.

Propionate attenuated pain behaviors in MIA-induced OA rats.

• A monosodium iodoacetate (MIA)-induced OA rat model was used to evaluate the effects of propionate on pain and inflammation.
• Behavioral assessments were used to measure pain outcomes.
• Propionate treatment improved pain behaviors compared to untreated OA rats.
• Nociceptive markers were reduced following propionate treatment.

Propionate preserved cartilage structure and reduced inflammatory markers in MIA-induced OA rats.

• Histological analysis was used to assess cartilage structure in MIA-induced rats.
• Propionate treatment preserved cartilage structure compared to OA controls.
• Both nociceptive and inflammatory markers were reduced with propionate treatment.
• Findings were assessed through histological analysis of joint tissue.

Propionate restored intestinal barrier function in MIA-induced OA rats.

• The intestinal environment was assessed by histology and tight junction protein analysis.
• Propionate treatment restored intestinal barrier function in OA rats.
• Tight junction protein expression was analyzed to evaluate barrier integrity.
• Results indicate propionate acts on the gut-joint axis to influence OA progression.

Propionate rebalanced gut microbiota composition in MIA-induced OA rats.

• Gut microbiota profiling was performed in MIA-induced rats with and without propionate treatment.
• Propionate treatment restored microbial balance in OA rats.
• Dysregulation of the gut-joint axis was identified as a contributor to OA progression.
• Microbiota characterization confirmed compositional changes associated with propionate treatment.

Propionate modulated inflammatory and extracellular matrix (ECM)-related gene expression in human OA chondrocytes stimulated with IL-1β.

• Human OA chondrocytes were analyzed using qPCR and RNA sequencing following IL-1β stimulation with or without propionate treatment.
• Propionate upregulated ECM-related genes in human OA chondrocytes.
• Propionate downregulated inflammatory mediators in IL-1β-stimulated human OA chondrocytes.
• RNA sequencing was used to comprehensively profile gene expression changes.

Propionate promoted autophagy and suppressed catabolic and inflammatory cell death pathways in human OA chondrocytes.

• Autophagy promotion was identified through gene expression analysis in human OA chondrocytes treated with propionate.
• Propionate suppressed catabolic pathways in IL-1β-stimulated human OA chondrocytes.
• Inflammatory cell death pathways were also suppressed by propionate treatment.
• These effects were identified via qPCR and RNA sequencing analyses.