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

Fig. 5. SA regulates IRE1α-mediated ER stress by IRE1α-IκBα-p65 signaling.

Fig. 5

a WB analysis for detecting IRE1α and downstream gene expression at the protein level. The ER stress-associated proteins GRP78, pIRE1α, IRE1α, p-IκBα, t-IκBα, p-p65 and p65 were detected in each group (i). Quantitative analysis of GRP78 (ii), the ratio of p-IRE1α/t-IRE1α (iii), the ratio of p-IκBα/t-IκBα (iv), and the ratio of p-p65/t-p-p65 (v) at the protein level. GAPDH was used as a reference protein (n = 3, one-way ANOVA). b P65 nuclear translocation in each treatment group. IF was used to detect p-65 in the nucleus, and DAPI was used to stain the cell nucleus; scale bar: 50 μm. c The IRE1α inhibitor APY29 blocked TNF-α-mediated ER stress. Chondrocytes were stimulated with TNF-α and then treated with 10 μM SA or 10 μM APY29 for 48 h. XPB1u and XPB1s were detected by RT-QPCR (i), and XPB1s, MMP13, GRP78, IRE1α, p-IRE1α, p-p65 and p65 were detected by WB analysis (ii). Quantitative analysis of XPB1s (iii), MMP13 (iv), GRP78 (v), the ratio of p-IRE1α/t-IRE1α (vi), and the ratio of p-p65/t-p65 (vii) at the protein level. GAPDH was used as a reference protein (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.