Figures & data
Figure 1. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced mitochondrial dysfunction. (A) Mitochondrial membrane potential was measured by TMRM; (B) Intracellular ATP levels were determined by a luciferase assay (*, #, $, p < .01).
Figure 2. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced oxidative stress. (A) The lipid peroxidation 4-HNE was determined by immunostaining; (B). NOX-4 was determined by western blot analysis (*, #, $, p < .01).
Figure 3. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced expression of MMP-3 and MMP-13. (A) Expression of MMP-3 and MMP-13 determined by real-time PCR analysis; (B) Expression of MMP-3 and MMP-13 determined by western blot analysis (*, #, $, p < .01).
Figure 4. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced degradation of type II collagen. Type II collagen was determined by western blot analysis (*, #, $, p < .01).
Figure 5. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced expression of ADAMTS-4 and ADAMTS-5. (A) Expression of ADAMTS-4 and ADAMTS-5 were determined by real-time PCR analysis; (B) Expression of ADAMTS-4 and ADAMTS-5 were determined by western blot analysis (*, #, $, p < .01).
Figure 6. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced degradation of aggrecan. Aggrecan was determined by western blot analysis (*, #, $, p < .01).
Figure 7. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced secretion of TNF-α and IL-6. (A) Expression of TNF-α and IL-6 at the gene level was determined real-time PCR analysis; (B) Secretion of TNF-α and IL-6 at the protein level was determined ELISA (*, #, $, p < .01).
Figure 8. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced phosphorylation and degradation of IκBα. Phosphorylated and total levels of IκBα were determined by western blot analysis (*, #, $, p < .01).
Figure 9. Lixisenatide ameliorates advanced glycation end products (AGEs)-induced activation of NF-κB. (A) Nuclear translocation of p65; lamin B was used as a positive control; (B) Luciferase activity of NF-κB (*, #, $, p < .01).
