Fig. 8

Pharmacological inhibition on the NF-κB/NLRP3 axis attenuates CEP degeneration in cKO mice following LSI. a A schematic graph illustrates the experimental design. The cKO mice at 8 weeks of age were treated with tamoxifen for 5 consecutive days to induce Spp1 knockout and at 9 weeks of age, the mice were randomized and subjected to a sham or LSI surgery. Subsequently, the LSI cKO mice were treated intraperitoneally with vehicle or MCC950 and CAPE (C/M) every three days for 8 weeks. b μCT (top) and reconstruction (bottom) images of the coronal plane of lumbar endplates in cKO mice. Quantification of μCT analyses for DHI (c) and the porosity (d) of mouse lumbar endplates in cKO mice (n = 5). SO-FG staining (e) and histological scores (f) of lumbar EP in cKO mice (n = 5). g–i IHC staining and quantification of Aggrecan and MMP13 expression in CEP tissues from cKO mice (n = 5). j–l WB analyses of Aggrecan, MMP13, CCL2, CCL5, NLRP3, cleaved Caspase1, and cleaved IL-1β expression in CEP tissues from cKO mice (n = 3). m A schematic illustration of the mechanism by which OPN deficiency influences CEP homeostasis by enhancing the NF-κB signaling during the process of IDD. *P < 0.05, **P < 0.01, ***P < 0.001