• Xiaosheng Fan, Yan Yang, and Lin Qi.
• Department of Cardiology, Jinan People's Hospital Affiliated to Shandong First Medical University, Jinan, China - lwfanxsh@163.com.
• Minerva Med. 2023 Apr 1; 114 (2): 210216210-216.

BackgroundThe 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.MethodsH/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. Viability, 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 transcriptional activity of nuclear factor-κB (NF-κB) was measured by luciferase assay.ResultsH/R resulted in upregulation of DPP-4 and Nox-4, as well as increased LDH release in CMECs. In addition, 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 activation of the p38/NF-κB signaling in H/R-induced CMECs.ConclusionsVildagliptin protects CMECs from H/R injury via inactivating the p38/NF-κB signaling.

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