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Fig. 1 | Arthritis Research & Therapy

Fig. 1

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. 1

Evaluation of altered glycopatterns in cartilage from OA patients. a, b The morphology of the articular knee joint was assessed by X-ray imaging. Compared with the normal control (a), the joint space, and morphology of OA patients (b) were altered. c, d The articular cartilage from normal controls (c) and OA patients (d) was evaluated for histopathologic features using H&E staining. e, f Safranine-O staining was used to assess the degenerative degree of cartilage sections in normal control (e) and OA patients (f) (original magnification ×100). g, h Scanned images were obtained for the analysis of glycopatterns of articular cartilage from OA patients (g) and normal controls (h). i The lectins with increased NFIs in OA patients are marked with red boxes, and those with decreased NFIs are marked with white boxes. The NFIs of 15 lectins were significantly changed in OA patients (n=12) compared with normal controls (n=11) based on fold change and t test, and the data are presented as the average NFI ± SEM (*p < 0.05, **p < 0.01, and ***p < 0.001). j Lectin blotting of PSA, LTL, and AAL was performed to validate the differential expression of the glycopatterns in cartilage from OA patients and normal controls. The differential protein bands between OA patients and normal controls are marked with red frames. k The gray value of the difference protein bands was measured using ImageJ software and compared by t test (*p < 0.05, **p < 0.01, and ***p < 0.001)

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