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Fig. 3 | Arthritis Research & Therapy

Fig. 3

From: Elevation of α-1,3 fucosylation promotes the binding ability of TNFR1 to TNF-α and contributes to osteoarthritic cartilage destruction and apoptosis

Fig. 3

Suppression of fucosylation impeded ECM degradation and cell senescence. a The α-1,3/6 fucosylation levels identified by AAL, LTL, and PSA were markedly elevated in chondrocytes induced by TNF-α compared with the control and were significantly inhibited by 2FPF. b Effect of the fucosylation synthesis inhibitor 2FPF alone or in combination with TNF-α on the inducible expression of COL2A1 and MMP-13. β-Tubulin was used as an internal control. c The gray value of each protein band was extracted from three experimental replications. The expression of MMP-13 and COL2A1 was normalized to that of β-tubulin and compared between groups using one-way ANOVA. d SA-β-Gal staining was used to assess the effect of 2FPF on cell senescence induced by TNF-α; scale bar =20 μm. e The number of SA-β-Gal-positive cells in chondrocytes treated with or without TNF-α and the presence or absence of 2FPF was counted in 5 random fields. f The effect of 2FPF on the viability of normal and TNF-α-treated chondrocytes (n = 4). The data are presented as the mean ± SEM, *p < 0.05, **p < 0.01, and ***p < 0.001

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