Vildagliptin protects hypoxia/reoxygenation-induced injury of cardiac microvascular endothelial cells

BACKGROUND: The aim of this study was to uncover the protective role of Vildagliptin in hypoxia-reoxygenation (H/R)-induced injury of cardiac microvascular endothelial cells (CMECs) and the pharmacological mechanisms.METHODS: H/R model was constructed in primary CMECs extracted from rats, followed by Vildagliptin treatment. Relative levels of DPP-4 and Nox-4 in CMECs were detected by quantitative real-time polymerase chain reaction. Vi-ability, glutathione (GSH) content, lactate dehydrogenase (LDH) release and inflammatory factor levels were examined. Western blot was conducted to detect protein levels of DPP-4, p38, p-p38 and nuclear translocation of p65. The transcrip-tional activity of nuclear factor-kappa B (NF-kappa B) was measured by luciferase assay.RESULTS: H/R resulted in upregulation of DPP-4 and Nox-4, as well as increased LDH release in CMECs. In addi-tion, GSH content and viability were declined, and the release of inflammatory factors were stimulated in H/R-induced CMECs. The abovementioned changes were relieved by Vildagliptin treatment. Vildagliptin markedly inhibited the acti-vation of the p38/NF-kappa B signaling in H/R-induced CMECs.CONCLUSIONS: Vildagliptin protects CMECs from H/R injury via inactivating the p38/NF-kappa B signaling.(Cite this article as: Fan X, Yang Y, Qi L. Vildagliptin protects hypoxia/reoxygenation-induced injury of cardiac microvascu-lar endothelial cells. Minerva Med 2023;114:210-6. DOI: 10.23736/S0026-4806.20.06682-3)Key words: Vildagliptin; NF-kappa B; Myocardial infarction; Oxidative stress.