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Fig. 6 | Arthritis Research & Therapy

Fig. 6

From: Progranulin derivative Atsttrin protects against early osteoarthritis in mouse and rat models

Fig. 6

Atsttrin inhibits TNFα-induced catabolic metabolism. a Western blot analysis bands of phosphorylation and expression of indicated signaling molecules (p38, p-p38, JNK, p-JNK) at various time points. b Human primary chondrocytes cultured without or with 10 ng/ml TNFα in absence or presence of 200 ng/ml Atsttrin for various time points. Phosphorylation and expression of molecules of interest (NF-κB) determined by western blot analysis. c Representative image of immunohistochemistry staining for phosphorylated IkBα in the articular cartilage of WT ACLT-model mice. d Expression of p65 in primary chondrocyte cytoplasmic or nuclear extracts. Primary chondrocytes cultured without or with 10 ng/ml TNFα in presence or absence of 200 ng/ml Atsttrin. GAPDH and lamin B shown as cytoplasmic and nuclear internal controls, respectively. e Luciferase activity of NF-κB reporter gene. f Expression of MMP-3, MMP-13, ADAMTS-4, and NOS-2 analyzed by western blot assay. Primary human chondrocytes treated by 10 ng/ml TNFα without or with 200 ng/ml Atsttrin. Tubulin is internal control. gj Transcriptional levels of catabolic inflammatory biomarkers, including MMP-13, ADAMTS-4, NOS-2, and COX-2, in primary human chondrocytes. Values are normalized mean ± SEM. *p < 0.05, **p < 0.01 versus control group. Six cartilage samples used in each group. k Proposed model for demonstrating Atsttrin’s role and mechanism in OA. MMP matrix-degrading enzyme matrix metalloproteinase, PBS phosphate-buffered saline, TNFR tumor necrosis factor receptor, TNFα tumor necrosis factor alpha

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