Figures & data
Figure 1. Salicin treatment suppressed AGE-induced oxidative stress in human SW1353 chondrosarcoma cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Intracellular ROS was determined by the DCFH-DA assay; (B). The protein carbonyl content was determined by the 2, 4-dinitrophenyl-hydrazine (DNPH) assay (a, b, c, p < .01 vs. previous column group).
![Figure 1. Salicin treatment suppressed AGE-induced oxidative stress in human SW1353 chondrosarcoma cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Intracellular ROS was determined by the DCFH-DA assay; (B). The protein carbonyl content was determined by the 2, 4-dinitrophenyl-hydrazine (DNPH) assay (a, b, c, p < .01 vs. previous column group).](/cms/asset/694de337-76d3-457e-a8d8-469de906e2bf/ianb_a_1591427_f0001_c.jpg)
Figure 2. Salicin treatment suppressed the expression and secretions of pro-inflammatory cytokines. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Expressions of IL-1β, TNF-α, and MCP-1 at the mRNA levels were determined by real time PCR analysis; (B). Secretion of IL-1β, TNF-α, and MCP-1 was determined by ELISA.
![Figure 2. Salicin treatment suppressed the expression and secretions of pro-inflammatory cytokines. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Expressions of IL-1β, TNF-α, and MCP-1 at the mRNA levels were determined by real time PCR analysis; (B). Secretion of IL-1β, TNF-α, and MCP-1 was determined by ELISA.](/cms/asset/d5ee43c9-0850-488c-b19d-b12cb5d136d9/ianb_a_1591427_f0002_b.jpg)
Figure 3. Salicin treatment inhibited the secretion of high-mobility group protein 1 (HMGB-1). Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. Secretion of HMGB-1 was determined by the ELISA assay (a, b, c, p < .01 vs. previous column group).
![Figure 3. Salicin treatment inhibited the secretion of high-mobility group protein 1 (HMGB-1). Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. Secretion of HMGB-1 was determined by the ELISA assay (a, b, c, p < .01 vs. previous column group).](/cms/asset/ec8d04b4-f5ed-4074-900a-068202dfa952/ianb_a_1591427_f0003_b.jpg)
Figure 4. Salicin treatment ameliorated AGEs-induced degradation of type II collagen in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. Expression of type II collagen was determined by western blot analysis (a, b, c, p < .01 vs. previous column group).
![Figure 4. Salicin treatment ameliorated AGEs-induced degradation of type II collagen in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. Expression of type II collagen was determined by western blot analysis (a, b, c, p < .01 vs. previous column group).](/cms/asset/77c7a8fb-878a-4bbd-9cd4-feeb32b25349/ianb_a_1591427_f0004_b.jpg)
Figure 5. Salicin treatment ameliorated AGEs-induced expression of MMP-1, MMP-3, and MMP-13 in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Expression of MMP-1, MMP-3, and MMP-13 at the gene levels was determined by real time PCR analysis; (B). Expression of MMP-1, MMP-3, and MMP-13 at the protein levels was determined by ELISA (a, b, c, p < .01 vs. previous column group).
![Figure 5. Salicin treatment ameliorated AGEs-induced expression of MMP-1, MMP-3, and MMP-13 in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Expression of MMP-1, MMP-3, and MMP-13 at the gene levels was determined by real time PCR analysis; (B). Expression of MMP-1, MMP-3, and MMP-13 at the protein levels was determined by ELISA (a, b, c, p < .01 vs. previous column group).](/cms/asset/b6a46498-128a-4b70-903c-df5edf4fda6e/ianb_a_1591427_f0005_b.jpg)
Figure 6. Salicin treatment ameliorated AGEs-induced degradation of aggrecan in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. Expression of Aggrecan was determined by Western blot analysis (a, b, c, p < .01 vs. previous column group).
![Figure 6. Salicin treatment ameliorated AGEs-induced degradation of aggrecan in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. Expression of Aggrecan was determined by Western blot analysis (a, b, c, p < .01 vs. previous column group).](/cms/asset/739518c0-5171-442a-b064-f9b60a970372/ianb_a_1591427_f0006_b.jpg)
Figure 7. Salicin treatment ameliorated AGEs-induced expressions of ADAMTS-4 and ADAMTS-5 in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Expression of ADAMTS-4 and ADAMTS-5 at the gene levels was determined by real time PCR analysis; (B). Expression of ADAMTS-4 and ADAMTS-5 at the protein levels was determined by ELISA (a, b, c, p < .01 vs. previous column group).
![Figure 7. Salicin treatment ameliorated AGEs-induced expressions of ADAMTS-4 and ADAMTS-5 in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Expression of ADAMTS-4 and ADAMTS-5 at the gene levels was determined by real time PCR analysis; (B). Expression of ADAMTS-4 and ADAMTS-5 at the protein levels was determined by ELISA (a, b, c, p < .01 vs. previous column group).](/cms/asset/7a1c9db9-ff6d-40ed-b2c8-120ecba93fd7/ianb_a_1591427_f0007_b.jpg)
Figure 8. Salicin treatment inhibits AGEs-induced activation of NF-κB in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Nuclear translocation of p65; Lamin B was used as a positive control; (B). Luciferase activity of NF-κB was determined (a, b, c, p < .01 vs. previous column group).
![Figure 8. Salicin treatment inhibits AGEs-induced activation of NF-κB in human SW1353 cells. Human SW1353 cells were treated with 100 μg/ml AGEs in the presence or absence of 50 and 100 μM salicin for 48 h. (A). Nuclear translocation of p65; Lamin B was used as a positive control; (B). Luciferase activity of NF-κB was determined (a, b, c, p < .01 vs. previous column group).](/cms/asset/acb28494-c19c-4ba8-8d0f-9428c1f1feea/ianb_a_1591427_f0008_b.jpg)