Fig. 6.

The PKCK2/STAMP2/FSP27 axis confers articular chondrocytes resistance to lipotoxicity. a Representative western blots showing that DRB decreased the expression level of STAMP2 and FSP27 (n = 4). b Representative western blots showing that 30 μmol·L^-1 cilostazol reversed the 1.5 mmol·L^-1 oleate-induced downregulation of STAMP2 (n = 4). c Representative immunohistochemistry on cartilages obtained from OA model without surgery. Cilostazol markedly prevented the HFD-induced cartilage destruction. OARSI scoring demonstrated that cilostazol significantly reduced the degeneration of cartilage. **P < 0.01 according to Scheffe’s test. Cilostazol significantly increased the populations of PKCK2, STAMP2 or FSP27-positive cells irrespective of diet type (n = 4). **P < 0.01 vs. vehicle (V) administered experimental control mice according to Scheffe’s test. Scale bar, 20 μm. d Representative western blots showing that STAMP2 was efficiently overexpressed by Ad-STAMP2 in articular chondrocytes. Viability assay showing that overexpressed STAMP2 significantly prevented oleate-induced cell death. **P < 0.01 vs. 1.5 mmol·L^-1 oleate alone plus empty vector (Ad-EV) treatment according to Scheffe’s test. e Representative western blots showing that overexpressed STAMP2 (1 000 MOI) reversed the 1.5 mmol·L^-1 oleate-induced decrease in FSP27 protein expression levels (n = 4). f The overexpression of STAMP2 (1 000 MOI) reversed the 1.5 mmol·L^-1 oleate-induced reduction in the total LD volume. **P < 0.01 vs. empty vector according to Scheffe’s test. Scale bar, 10 μm