Research Paper Volume 11, Issue 19 pp 8664—8680

Figure 4. RIPK1 potentiates TIR-domain-containing adapter-inducing interferon b (TRIF)- and myeloid differentiation primary response 88 (MyD88)-dependent IL-β–induced inflammation. (A, B) Western blots and quantitative data of TRIF and MyD88 in chondrocytes transfected with Ad-shRIPK in the presence and absence of IL-1β. © Western blots of TRIF and MyD88 in chondrocytes transfected with si-TRIF or si-MyD88. (D, E) Western blots and quantitative data of MMPs in chondrocytes transfected with si-TRIF or si-MyD88 in the presence and absence of IL-1β. (F, G) Western blots and quantitative data of MMPs in chondrocytes incubated with poly (I:C) or Pam3CSK4 in the Ad-shRIPK and Ad-NC groups. (H, I) Western blots and quantitative data of MMPs in chondrocytes transfected with Ad-shRIPK adenovirus in the si-TRIF and si-MyD88 groups. (J, K) Western blots and quantitative data of p-RIPK1 in chondrocytes treated with IL-1β in the si-TRIF and si-MYD88 groups. The experiments were repeated three times independently. Columns represent means ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.