DPP-4 (CD26) inhibitor sitagliptin exerts anti-inflammatory effects on rat insulinoma (RINm) cells via suppressing NF-κB activation

Dipeptidyl peptidase-4 (CD26), a cell surface glycoprotein, is expressed by a variety of cells. It has been shown that dipeptidyl peptidase-4 (CD26) is involved in T cell activation. Nonetheless, its role in inflammatory effects in islet beta cells has not been well investigated. In this study, we used sitagliptin, a classic inhibitor of dipeptidyl peptidase-4 (CD26), to research the effect of dipeptidyl peptidase-4 (CD26) on the activation of NF-kappa B, the expression of inflammatory cytokines, and cell apoptosis in rat insulinoma cells. Results showed that dipeptidyl peptidase-4 (CD26) was expressed on the surface of rat insulinoma cells. Lipopolysaccharide-induced NF-kappa B activation and expression of inflammatory cytokines were suppressed by sitagliptin treatment in rat insulinoma cells. Furthermore, sitagliptin treatment reduced cell apoptosis stimulated by lipopolysaccharide. Taken together, this study showed for the first time that sitagliptin suppressed NF-kappa B activation and inflammatory cytokines expression in rat insulinoma cells, suggesting that the dipeptidyl peptidase-4 inhibitor may exert direct anti-inflammatory effects in islet beta cells.