Fig. 7: SA ameliorates ACLT-induced OA progression by inhibiting IRE1α-mediated ER stress in vivo. | Experimental & Molecular Medicine

Fig. 7: SA ameliorates ACLT-induced OA progression by inhibiting IRE1α-mediated ER stress in vivo.

From: The natural product salicin alleviates osteoarthritis progression by binding to IRE1α and inhibiting endoplasmic reticulum stress through the IRE1α-IκBα-p65 signaling pathway

Fig. 7

a P-IRE1α in chondrocytes in each treatment group. IF was used to detect p-IRE1α in each treatment group. p-IRE1α was highly expressed in the cytoplasm of chondrocytes in the ACLT and vehicle groups, and SA dramatically decreased the expression of p-IRE1α in the cytoplasm of chondrocytes (i). Quantitative analysis showed that ACLT-induced high expression of p-IRE1α was significantly reversed by SA treatment (ii) (n = 5, one-way ANOVA). b P-p65 nuclear translocation in each treatment group. ACLT-induced p-p65 nuclear translocation was ameliorated by SA treatment (i). Quantitative analysis of each treatment group showed the same trend (ii). Scale bar, 50 μm; the ACLT group indicates the group injected with PBS; the vehicle group indicates the group injected with only PLGA vehicle; the SA group indicates the group injected with SA-loaded PLGA. Dashed lines indicate the cartilage surface. The data are expressed as the mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, and ns, not significant. c A proposed model of action. SA binding to IRE1α blocked IRE1α phosphorylation and inhibited IRE1α-mediated ER stress via IRE1α-IκBα-p65 signaling.

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