Emodin Enhances Chondrogenic Differentiation Potential In Fibrocartilage Stem Cells

While emodin demonstrates osteochondral regenerative capacity in appendicular joints, its therapeutic potential in fibrocartilaginous temporomandibular joint (TMJ) remains underexplored. This study systematically investigated emodin's effects on fibrocartilage stem cells (FCSCs) for TMJ cartilage regeneration. FCSCs isolated enzymatically from Sprague-Dawley rat condylar cartilage were treated with emodin (2.5-20 μM) for 7 days. The CCK-8 assay was utilized for determining the viability of emodin-treated FCSCs. qRT-PCR analysis and Western blot were employed to measure the expression of osteogenic and chondrogenic markers. CCK-8 assays revealed dose-dependent proliferation enhancement (1.5-fold at 20 μM vs controls, p<0.01). qRT-PCR analysis showed marked upregulation of chondrogenic markers Sox9 (3.2±0.4-fold) and Aggrecan (2.8±0.3-fold), with concurrent suppression of adipogenic Ppar-γ (0.4±0.1-fold) and osteogenic Runx2 (0.6±0.2-fold) expression (p<0.05). Western blot confirmed protein-level increases in Sox9 (2.1-fold) and decreases in Runx2 (0.5-fold) at 20 μM treatment. These findings establish that emodin preferentially directs FCSCs differentiation toward chondrogenesis. The dose-responsive upregulation of cartilage-specific transcription factors coupled with extracellular matrix synthesis suggests emodin's therapeutic potential for TMJ cartilage regeneration. This study provides the first evidence of emodin's fibrocartilage-specific regenerative mechanisms, offering novel insights for temporomandibular disorder treatment strategies.