Linagliptin improved myocardial function recovery in rat hearts after a prolonged hypothermic preservation.

摘要: Abstract Aims To determine whether linagliptin, a dipeptidyl peptidase 4 inhibitor, can promote the recovery of cardiac function after hypothermic preservation. Main methods Rat hearts were preserved in cold Celsior solution with or without linagliptin for 9 h. Cardiac was evaluated at 60 min reperfusion mitochondrial morphology observed using transmission electron microscope. The expression dynamin-related protein 1 (Drp1), NADPH oxidase 2 (NOX2), calmodulin-dependent kinase II (CaMKII) detected Western blot. Key findings Compared group, supplement (0.25–0.75 nM) could significantly prevent preservation-induced dysfunction. NOX2 protein, ROS level and MDA content cardium increased preservation, which inhibited by linagliptin. Although mitofusin1, 2, optic atrophy type 1, total Drp1 myocardium did not change, p-Drp1 S616 enhanced Linagliptin inhibit increase mitigate fragmentation. Level p-CaMKII be prevented inhibitor Phox-I2. Both Phox-I2 CaMKII KN-93 reduce protein. Significance Supplement improve 9-h rat hearts. cardioprotective effect might due to inhibition phosphorylation translocation preventing NOX2-mediated activation.