Figures & data
Figure 1. The cytotoxicity of celecoxib in human C-28/I2 chondrocytes. Cells were treated with celecoxib at concentrations of 0, 1, 5, 10, 20, 100, 200 μM for 24 hours. (a) The molecular structure of celecoxib; (b) The effects of celecoxib in cell viability of human chondrocytes (*, **, P < 0.05, 0.01 vs. vehicle group)
![Figure 1. The cytotoxicity of celecoxib in human C-28/I2 chondrocytes. Cells were treated with celecoxib at concentrations of 0, 1, 5, 10, 20, 100, 200 μM for 24 hours. (a) The molecular structure of celecoxib; (b) The effects of celecoxib in cell viability of human chondrocytes (*, **, P < 0.05, 0.01 vs. vehicle group)](/cms/asset/08eeb044-9f4b-484b-9989-244f38657f13/kbie_a_2003661_f0001_oc.jpg)
Figure 2. Celecoxib reduced ROS production in TNF-α-challenged human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10 and 20 μM for 24 hours. ROS generation was labeled by green fluorescence (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)
![Figure 2. Celecoxib reduced ROS production in TNF-α-challenged human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10 and 20 μM for 24 hours. ROS generation was labeled by green fluorescence (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)](/cms/asset/6fa3e490-1060-4c3a-995a-64840cc53d2c/kbie_a_2003661_f0002_oc.jpg)
Figure 3. The effect of Celecoxib on the cell cycle arrest in the G0/G1 phase induced by TNF-α in human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 7 days. Cell cycle fraction in the G0/G1 phase, G2/M phase, and S phase was calculated (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)
![Figure 3. The effect of Celecoxib on the cell cycle arrest in the G0/G1 phase induced by TNF-α in human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 7 days. Cell cycle fraction in the G0/G1 phase, G2/M phase, and S phase was calculated (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)](/cms/asset/b11752f4-bd03-4c2d-9d8c-276f68a8728c/kbie_a_2003661_f0003_oc.jpg)
Figure 4. The effect of Celecoxib on the telomerase activity in TNF-α-challenged human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 7 days. The telomerase activity was detected using a chemical kit (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)
![Figure 4. The effect of Celecoxib on the telomerase activity in TNF-α-challenged human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 7 days. The telomerase activity was detected using a chemical kit (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)](/cms/asset/9ef332e2-36ac-4f27-acaa-65c77100a86e/kbie_a_2003661_f0004_oc.jpg)
Figure 5. Celecoxib ameliorated cellular senescence against TNF-α in human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 7 days. The SA-β-Gal activity was determined (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)
![Figure 5. Celecoxib ameliorated cellular senescence against TNF-α in human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 7 days. The SA-β-Gal activity was determined (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)](/cms/asset/0b9625f4-4805-4b2c-9ff8-ec9046454fa8/kbie_a_2003661_f0005_oc.jpg)
Figure 6. The effect of Celecoxib on the activation of p-ATM and p-CHK2 induced by TNF-α in human chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at the concentrations of 10, 20 μM for 6 hours. The expressions of p-ATM/ATM and p-CHK2/CHK2 were detected using western blots (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)
![Figure 6. The effect of Celecoxib on the activation of p-ATM and p-CHK2 induced by TNF-α in human chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at the concentrations of 10, 20 μM for 6 hours. The expressions of p-ATM/ATM and p-CHK2/CHK2 were detected using western blots (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)](/cms/asset/a1291861-bb20-44ad-ad6c-cdd2fd4d7372/kbie_a_2003661_f0006_oc.jpg)
Figure 7. The effect of Celecoxib on the increased expression of p21 and p53induced by TNF-α in human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 6 hours. The expressions of p21 and p53 were detected using western blots (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)
![Figure 7. The effect of Celecoxib on the increased expression of p21 and p53induced by TNF-α in human C-28/I2 chondrocytes. Cells were treated with TNF-α (10 ng/ml) in the absence or presence of Celecoxib at concentrations of 10, 20 μM for 6 hours. The expressions of p21 and p53 were detected using western blots (***, P < 0.005 vs. vehicle group; #, ##, P < 0.05, 0.01 vs. TNF-α group)](/cms/asset/ec8df384-50c0-4249-81b2-048237e03bb6/kbie_a_2003661_f0007_oc.jpg)
Data availability statement
Requests for data and materials should be addressed to the corresponding author.