Minerva Medica 2020 Jul 20

DOI: 10.23736/S0026-4806.20.06682-3

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

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

Xiaosheng FAN ¹ ✉, Yan YANG ², Lin QI ³

¹ Department of Cardiology, Jinan People's Hospital Affiliated to Shandong First Medical University, Jinan, China; ² Department of Health Examination Center, Qilu Hospital of Shandong University, Jinan, China; ³ Department of Internal Medicine, Jinan People's Hospital Affiliated to Shandong First Medical University, Jinan, China

BACKGROUND: 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 (qRT-PCR). 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.
RESULTS: H/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.
CONCLUSIONS: Vildagliptin protects CMECs from H/R injury via inactivating the p38/NF-κB signaling.

KEY WORDS: Vildagliptin; H/R; NF-κB; Myocardial infarction; Oxidative stress