Figure 3
Figure 3. Antagonizing TNFα with a monoclonal antibody (TNFαmAb) cannot protect cartilage from blood-induced damage. (A) Healthy human cartilage (n = 3) was cultured for 4 days in the absence (control; dotted line) or presence of TNFα and TNFαmAb. Proteoglycan synthesis rate was determined to check the activity of the antibody. (B) Cartilage was cultured in the absence (control; 100% level) or presence of whole blood (50% v/v) with/without TNFαmAb (10 μg/mL) (n = 5). Proteoglycan turnover was determined after 12 days of recovery. *P < .05 compared with control values. No statistically significant effects between cultures with and without TNFαmAb were seen.

Antagonizing TNFα with a monoclonal antibody (TNFαmAb) cannot protect cartilage from blood-induced damage. (A) Healthy human cartilage (n = 3) was cultured for 4 days in the absence (control; dotted line) or presence of TNFα and TNFαmAb. Proteoglycan synthesis rate was determined to check the activity of the antibody. (B) Cartilage was cultured in the absence (control; 100% level) or presence of whole blood (50% v/v) with/without TNFαmAb (10 μg/mL) (n = 5). Proteoglycan turnover was determined after 12 days of recovery. *P < .05 compared with control values. No statistically significant effects between cultures with and without TNFαmAb were seen.

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