Fig. 4: TEPP-46 inhibits PKM2 dimer formation and maintains ECM metabolism homeostasis in vitro.

a Representative immunoblots and b densitometric quantification of tetrameric and dimeric PKM2 in cartilage tissues from non-OA (n = 4) and OA (n = 6) patients. Data were presented as means ± s.e.m., unpaired Student’s t-test. c Representative immunoblots and d densitometric quantification of tetrameric and dimeric PKM2 in chondrocytes treated with vehicle, DASA-58 (2, 10, and 50 μM) or TEPP-46 (10 and 50 μM) for 48 h in the presence of IL-1β, in a dose-dependent manner. Data were presented as means ± s.e.m., n = 6, one-way ANOVA with Tukey’s multiple comparisons. e Representative IF images of PKM2 in chondrocytes treated with 50 μM TEPP-46 for 48 h. f Representative immunoblots and g densitometric quantification of ADAMTS5, MMP3, MMP13, and COL2A1 in IL-1β-stimulated chondrocytes treated with TEPP-46 (10 and 50 μM) for 48 h. Data were presented as means ± s.e.m., n = 6, one-way ANOVA with Tukey’s multiple comparisons. h Representative SO&FG staining and i quantification of cartilage area in mouse femur head stimulated ex vivo with IL-1β (10 ng mL⁻¹) and treated with 50 μM TEPP-46 for 7 days. Data were presented as means ± s.e.m., n = 6, one-way ANOVA with Tukey’s multiple comparisons. *P < 0.05, **P < 0.01. ns not significant.