Research Paper Volume 13, Issue 14 pp 19013—19027

Glucagon-like peptide-1 attenuated carboxymethyl lysine induced neuronal apoptosis via peroxisome proliferation activated receptor-γ

PPAR-γ inhibition abolished the protective effect of GLP-1 on PC12 cells from apoptosis induced by CML. Results in (A) showed GW9662 abolished the protective effect of GLP-1 on PC12 cells from apoptosis induced by CML. (B) Showed the western blotting results of bcl2, bax, and GLP-1R. “a” in (C) showed the down-regulated bcl2 and GLP-1R as well as up-regulated bax levels between PC12 cells (treated by 50ug/ml CML and 100 nM GLP-1) with and without 5uM GW9662. Results in (D) showed the direct interactivity between PPAR-γ and GLP-1R promoter sequence. Data are represented as mean ± SD; n = 3 per group for results of western blotting.

Figure 2. PPAR-γ inhibition abolished the protective effect of GLP-1 on PC12 cells from apoptosis induced by CML. Results in (A) showed GW9662 abolished the protective effect of GLP-1 on PC12 cells from apoptosis induced by CML. (B) Showed the western blotting results of bcl2, bax, and GLP-1R. “a” in (C) showed the down-regulated bcl2 and GLP-1R as well as up-regulated bax levels between PC12 cells (treated by 50ug/ml CML and 100 nM GLP-1) with and without 5uM GW9662. Results in (D) showed the direct interactivity between PPAR-γ and GLP-1R promoter sequence. Data are represented as mean ± SD; n = 3 per group for results of western blotting.