Insulin-Attenuated Inflammatory Response of Dendritic Cells in Diabetes by Regulating RAGE-PKCβ1-IRS1-NF-κB Signal Pathway: A Study on the Anti-Inflammatory Mechanism of Insulin in Diabetes

Figure 7

AGEs-BSA-stimulating DCs to increase RAGE expression, followed by promoted phosphorylation of PKCβ1 and serine phosphorylated IRS1 and activated NF-κB and upregulated proinflammatory genes; insulin therapy attenuating AGEs-BSA-induced inflammatory response of DCs partly by inhibiting RAGE expression, dephosphorylation of PKCβ1, and serine residue of IRS1.