Background: Cardiovascular diseases and cancer remain leading causes of mortality in the world. Doxorubicin (DOX) treatment is the primary cause of chemotherapy-induced cardiotoxicity. Sitagliptin (STG) has been shown to improve cardiovascular functions. Endothelial nitric oxide synthase (eNOS) is the major weapon of endothelial cells to fight vascular diseases as it generates nitric oxide (NO). Aim: The aim of this study was to evaluate the cardiotoxic effect of DOX on heart of adult male albino rats and the possible role of STG, targeting the role of eNOS. Methods: The effect of DOX on albino rats was studied by estimating systolic blood pressure (SBP) , diastolic blood pressure (DBP) , E.C.G recording, Serum levels of creatine phosphokinase MB (CK-MB), lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA), cardiac tissue level of NO. Results: DOX injection resulted in significant increases in both SBP and DBP, significant ST segment elevation and significant increases in serum levels of CK-MB, LDH and MDA associated with significant decreases in heart rate, cardiac NO levels and serum SOD levels as compared with the control group. STG administration reversed the aforementioned parameters. STG administration with NG-Nitro arginine methyl ester (L-NAME) and DOX reverse STG protective effects. Conclusion: STG administration can exert protective effects against doxorubicin induced cardiac toxicity through the increase in cardiac NO and e-NOS while its administration with L-NAME reverse these effects. |
