Skip to main content
Figure 1 | Cardiovascular Diabetology

Figure 1

From: Exenatide can inhibit calcification of human VSMCs through the NF-kappaB/RANKL signaling pathway

Figure 1

Exenatide and RANKL-siRNA attenuate osteoblastic differentiation and calcification of human CVSMCs. A) Representative Western blot of RANKL protein levels in human CVSMCs transfected with control siRNA (C-siRNA) or R-siRNA for 48 hours. B) Exenatide inhibited ALP activities in β-GP-treated VSMCs in a dose-dependent manner. VSMCs were treated for 48 hrs. N = 5, **P <0.001 vs. control (0 concentration of exenatide). C) Exenatide inhibited OC levels in β-GP-treated VSMCs in a dose-dependent manner. VSMCs were treated for 48 hrs. N = 5, **P <0.001 vs. 0 concentration of exenatide. D) Representative Western blot of ALP and RANKL protein expressions. Human CVSMCs were treated with or without exenatide (2 nM) and RANKL-siRNA (R-siRNA) for 48 h. GAPDH was used as the loading control. E) Semi-quantitative analysis of bands in Western blot at 48 hrs in each group. Bars represent meanmean ± SD. #P < 0.001 between two indicated groups. N = 5. F) Representative Alizarin Red S staining. Human CVSMCs were treated with various agents for 15 days. Magnificationmean ± 200. G) Quantification of Alizarin red S staining. The dye was extracted and quantified as described in the Method section. Bars represent meanmean ± SD. #P < 0.001 between two indicated groups. N = 5.

Back to article page