Fig. 2

Effect of PPARγ protein upregulation and PPARγ activation on an IDD cell model. HNPCs were treated with IL-1β (and pioglitazone) and /or transfected plasmid PPARγ (groups: NC, IL-1β, IL-1β + PPARγ, IL-1β + pioglitazone, IL-1β + PPARγ + pioglitazone). A The protein level of PPARγ was detected by Western blot. B Concentration of IL-6 in culture medium was detected by ELISA assay. C, D Protein expression of Col II, aggrecan, MMP3, MMP13, ADAMT-4, and ADAMT-5 in the ECM was detected by Western blot. E, F Flow cytometry analysis with Annexin V-PI staining was performed to evaluate the percentage of apoptotic cells in HNPCs. (*P < 0.05, **P < 0.01, ***P < 0.001 vs. NC group; ^#P < 0.05, ^###P < 0.001 vs. IL-1β group; ^{^}P < 0.05 vs. IL-1β + PPARγ group; ^&P < 0.05 vs. IL-1β + pioglitazone group). PPARγ, peroxisome proliferator-activated receptor γ; NC, normal control; IL, interleukin; Col II, type II collagen; MMP, matrix metalloproteinase; ADAMT, A disintegrin and metalloproteinase with thrombospondin motifs; PI, propidium iodide; FITC, fluorescein isothiocyanate; IDD, intervertebral disc degeneration; HNPCs, human nucleus pulposus cells; ELISA, enzyme-linked immunosorbent assay; ECM, extracellular matrix