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Proteintech tlr4 inhibitor tak
Dependence of CIRP-induced chondrocyte damage on <t>TLR4/NF-κB</t> signaling. (A) Cytotoxicity of BAY 11-7082 and TAK-242 on chondrocytes at various concentration for 48 h, assessed using a CCK-8 assay. (B and C) Western blotting showing the protein expression of IκBα in chondrocytes and p65 in the nucleus of chondrocytes following treatment with the two inhibitors. (D and E) Western blotting showing the protein expression NLRP3, cleaved-caspase-1, ASC and IL-1β following treatment with the two inhibitors. (F and G) Western blotting showing the expression of extracellular matrix proteins in chondrocytes following treatment with the two inhibitors. n=3, * P<0.05, ** P<0.01, *** P<0.001. CIRP, cold-inducible RNA-binding protein; TLR4, Toll-like receptor 4; NLRP3, NLR family pyrin domain containing 3; Cle, cleaved.
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Dependence of CIRP-induced chondrocyte damage on TLR4/NF-κB signaling. (A) Cytotoxicity of BAY 11-7082 and TAK-242 on chondrocytes at various concentration for 48 h, assessed using a CCK-8 assay. (B and C) Western blotting showing the protein expression of IκBα in chondrocytes and p65 in the nucleus of chondrocytes following treatment with the two inhibitors. (D and E) Western blotting showing the protein expression NLRP3, cleaved-caspase-1, ASC and IL-1β following treatment with the two inhibitors. (F and G) Western blotting showing the expression of extracellular matrix proteins in chondrocytes following treatment with the two inhibitors. n=3, * P<0.05, ** P<0.01, *** P<0.001. CIRP, cold-inducible RNA-binding protein; TLR4, Toll-like receptor 4; NLRP3, NLR family pyrin domain containing 3; Cle, cleaved.

Journal: International Journal of Molecular Medicine

Article Title: Targeting of CIRP attenuates osteoarthritis progression via suppressing TLR4/NF-κB/NLRP3 signaling axis

doi: 10.3892/ijmm.2025.5674

Figure Lengend Snippet: Dependence of CIRP-induced chondrocyte damage on TLR4/NF-κB signaling. (A) Cytotoxicity of BAY 11-7082 and TAK-242 on chondrocytes at various concentration for 48 h, assessed using a CCK-8 assay. (B and C) Western blotting showing the protein expression of IκBα in chondrocytes and p65 in the nucleus of chondrocytes following treatment with the two inhibitors. (D and E) Western blotting showing the protein expression NLRP3, cleaved-caspase-1, ASC and IL-1β following treatment with the two inhibitors. (F and G) Western blotting showing the expression of extracellular matrix proteins in chondrocytes following treatment with the two inhibitors. n=3, * P<0.05, ** P<0.01, *** P<0.001. CIRP, cold-inducible RNA-binding protein; TLR4, Toll-like receptor 4; NLRP3, NLR family pyrin domain containing 3; Cle, cleaved.

Article Snippet: TLR4 inhibitor TAK-242 was purchased from Shanghai Xianding Biotechnology Co., Ltd. Primary antibodies directed against inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), MMP1, MMP3, MMP13, Lamin B1, CD63, CD9, 130 kDa cis-Golgi matrix protein 1 (GM130) and GAPDH were purchased from Proteintech Group, Inc., ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5) was purchased from ABclonal.

Techniques: Concentration Assay, CCK-8 Assay, Western Blot, Expressing, RNA Binding Assay

Schematic illustration of targeting of CIRP attenuates osteoarthritis progression and the underlying mechanism. CIRP can be secreted in the form of exosomes and acts as a pro-inflammatory factor that activates the TLR4/NF-κB/NLRP3 signaling pathway, promoting the inflammatory response, ECM degradation and the progression of OA. Additionally, CIRP is identified as a target of miR-145, which inhibits its expression in OA. CIRP, cold-inducible RNA-binding protein; TLR4, Toll-like receptor 4; NLRP3, NLR family pyrin domain containing 3; OA, osteoarthritis; ECM, extracellular matrix; miR, microRNA; iNOS, inducible nitric oxide synthase; COX-2, cyclooxygenase-2; MMPs, matrix metalloproteinases.

Journal: International Journal of Molecular Medicine

Article Title: Targeting of CIRP attenuates osteoarthritis progression via suppressing TLR4/NF-κB/NLRP3 signaling axis

doi: 10.3892/ijmm.2025.5674

Figure Lengend Snippet: Schematic illustration of targeting of CIRP attenuates osteoarthritis progression and the underlying mechanism. CIRP can be secreted in the form of exosomes and acts as a pro-inflammatory factor that activates the TLR4/NF-κB/NLRP3 signaling pathway, promoting the inflammatory response, ECM degradation and the progression of OA. Additionally, CIRP is identified as a target of miR-145, which inhibits its expression in OA. CIRP, cold-inducible RNA-binding protein; TLR4, Toll-like receptor 4; NLRP3, NLR family pyrin domain containing 3; OA, osteoarthritis; ECM, extracellular matrix; miR, microRNA; iNOS, inducible nitric oxide synthase; COX-2, cyclooxygenase-2; MMPs, matrix metalloproteinases.

Article Snippet: TLR4 inhibitor TAK-242 was purchased from Shanghai Xianding Biotechnology Co., Ltd. Primary antibodies directed against inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), MMP1, MMP3, MMP13, Lamin B1, CD63, CD9, 130 kDa cis-Golgi matrix protein 1 (GM130) and GAPDH were purchased from Proteintech Group, Inc., ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5) was purchased from ABclonal.

Techniques: Expressing, RNA Binding Assay