Fig 1.
Diagrammatic representation of the curcumin role on inflammation and Col2 degradation.
The curcumin decreases lipo-oxygenase, mitogenic activation, JAK (Janus Kinase), IHH (Indian hedghog) and also COX-2 (cyclo-oxygenase-2) via NF-ΚB inhibition. The curcumin induces SOX-5 and iNOS (induced nitric oxide synthase). The curcumin inhibit MAPK (mitogen-activated protein kinase), MCP (monocyte chemoattractant protein), STAT (signal transduction and activation transcription), PI3K (phosphoinositide 3-kinase), MIP (Migration inhibitory protein). The expression of IL-1, 2, 6, 8 and 12 (interleukin), TNF-α (Tumour Necrosis Factor alpha) and IL-1β are inhibited via NF-ΚB (nuclear factor kappa B) inhibition. The MMP-1, 3, 8, 9 and 13 (matrix metalloproteinases) are mainly inhibited via TNF-α and IL-1β inhibition which leads to an inhibition in Col2 degradation.
Fig 2.
Photomicrographs of histological sagittal sections of the rat femoral articular cartilage.
Images of articular cartilage from the COAG (A), CG (B), and OAG (C) stained with HE; the surface, middle, and deep layers were observed. Immunohistochemical staining for Col2 was observed in the layers (surface, middle, and deep) of articular cartilage in the COAG (D), CG (E), and OAG (F) and IHH expression was detected in the layers of articular cartilage in the COAG (G), CG (H), and OAG (I). HE scale bar: 200 μm, immunohistochemistry scale bar: 50 μm.
Fig 3.
Quantification of Col2 expression.
Col2 expression in the surface layer was significantly different when the CG and COAG were compared with the OAG (p = 0.0332 and p = 0.00001, respectively). Col2 was expressed at significantly different levels in the middle layer of the CG and COAG compared with that in the OAG (p = 0.00002 and p = 0.00001, respectively). Significant differences in Col2 expression in the deep layer were observed between the CG and OAG and between the COAG and OAG (p = 0.0002 and p = 0.00001, respectively); p<0.05.
Fig 4.
Quantification of IHH expression.
Significant differences in IHH expression in the surface and deep layers were not observed between the CG, COAG and OAG. The CG and COAG displayed significant differences in IHH expression in the middle layer compared with that in the OAG (p = 0.00001 and p = 0.0202, respectively); p<0.05.
Fig 5.
Photomicrographs of immunohistochemical staining for MMP-8, MMP-13 and SOX-5.
MMP-8 expression was observed in the layers (surface, middle, and deep) of articular cartilage in the COAG (A), CG (B), and OAG (C). MMP-13 expression was detected in the layers of articular cartilage in the COAG (D), CG (E), and OAG (F). SOX-5 was expressed in the layers of articular cartilage in the COAG (G), CG (H), and OAG (I). Scale bar: 50 μm.
Fig 6.
Quantification of MMP-8 expression.
The COAG showed a significant difference in MMP-8 expression in the surface layer compared with that in the OAG (p = 0.0001). The CG displayed a significant difference in MMP-8 expression in the middle layer compared with that in the COAG (p = 0.0243). The CG and COAG showed significant differences in MMP-8 expression in the deep layer compared with that in the OAG (p = 0.0005 and p = 0.0293, respectively); p<0.05.
Fig 7.
Quantification of MMP-13 expression.
The COAG exhibited a significant difference in MMP-13 expression on the surface layer compared with that in the OAG (p = 0.0011). The CG showed a significant difference in MMP-13 expression in the middle and deep layers compared with that in the OAG (p = 0.0043 and p = 0.0007, respectively); p<0.05.
Fig 8.
Quantification of SOX-5 expression.
The COAG showed a significant difference in SOX-5 expression in the surface layer compared with that in the OAG (p = 0.0180). Significant differences in SOX-5 expression in the middle layer were not observed among the CG, COAG, and OAG. The CG displayed a significant difference in SOX-5 expression in the deep layer compared with that in the COAG (p = 0.0171); p<0.05.
Fig 9.
Articular cartilage thickness.
Significant differences in the thickness of the articular cartilage in the surface layer were not observed among the CG, COAG, and OAG. The CG displayed a significant difference in the thickness of the middle layer compared with those in the COAG and OAG (p = 0.0009 and p = 0.00001, respectively), and the COAG showed a significant difference in the thickness of the middle layer compared with that in the OAG (p = 0.00001). The CG displayed a significant difference in the thickness of the deep layer compared with those in the COAG and OAG (p = 0.0001 and p = 0.00001, respectively), and the COAG showed a significant difference in the thickness of the deep layer compared with that in the OAG (p = 0.0190); p<0.05.
Fig 10.
Chondrocyte counts in each layer.
The COAG showed a significantly different number of chondrocytes in the surface layer compared with that in the OAG (p = 0.0097). A significant difference in the number of chondrocytes in the middle layer was observed between the CG and the COAG and OAG (p = 0.0366 and p = 0.0002, respectively). Significant differences in the numbers of chondrocytes in the deep layer were not observed between the CG, COAG, and OAG; p<0.05.