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. 2022 Nov 10;54(11):1927–1939. doi: 10.1038/s12276-022-00879-w

Fig. 3. SA rescues TNF-α-induced inhibition of chondrocyte proliferation and TNF-α-induced promotion of chondrocyte apoptosis.

Fig. 3

a SA rescued TNF-α-induced inhibition of cell cycle marker expression at the mRNA level. Chondrocytes were stimulated with TNF-α and then treated with or without 10 μM SA for 48 h, and the relative mRNA expression levels of BCL2, CKD1, and MKi67 were detected (n = 3, one-way ANOVA). b Western blot analysis for detecting t-ERK and p-ERK in different groups treated with SA for 48 h (a). Quantitative analysis of the ratio of p-ERK/t-ERK. GAPDH was used as a reference protein (b) (n = 3, one-way ANOVA). c WB for detecting the proliferation markers BCL2 and CDK1 in different groups 48 hours after treatment at the protein level. Quantitative analysis of BCL2 (ii) and CDK1 (iii) at the protein level. GAPDH was used as a reference protein (n = 3, one-way ANOVA). d EdU assays for detecting DNA synthesis indicating cell proliferation with 24 h and 48 h treatment (i), scale bar 400 μm. Percentage of EdU (red)-positive staining at 24 h (ii) and 48 h (c) (n = 5, random fields, one-way ANOVA). e Flow cytometry for cell apoptosis analysis of chondrocytes in each treatment group at 24 h and 48 h (i). Percentage of apoptotic cells in each treatment group at 24 h (ii) and 48 h (c) (n = 3, one-way ANOVA). The data are expressed as the mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, and ns not significant.