Open Access

Sufentanil ameliorates oxygen‑glucose deprivation/reoxygenation‑induced endothelial barrier dysfunction in HCMECs via the PI3K/Akt signaling pathway

  • Authors:
    • Lianggang Wang
    • Chunlin Ge
    • Xinxin Zhang
  • View Affiliations

  • Published online on: May 11, 2022     https://doi.org/10.3892/etm.2022.11364
  • Article Number: 437
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ischemic heart disease, a chronic myocardial damage disease caused by coronary artery ischemia, is the leading cause of death worldwide. The aim of the present study was to explore the efficacy of sufentanil in myocardial ischemia/reperfusion (I/R) injury. Oxygen and glucose deprivation/reoxygenation (OGD/R) was utilized to induce human cardiac microvascular endothelial cells (HCMECs) to simulate myocardial I/R injury in vitro. The Cell Counting Kit‑8 assay was used to detect the effects of sufentanil on HCMECs and OGD/R‑induced HCMECs. The TUNEL, lactate dehydrogenase (LDH) activity, immunofluorescence and in vitro permeability assays, were used to assess apoptosis, LDH activity, VE‑cadherin protein expression levels and endothelial barrier function in OGD/R‑induced HCMECs, respectively. Moreover, western blotting was performed to assess the protein expression levels of apoptosis, endothelial barrier function and phosphatidylinositol‑3‑kinase (PI3K)/protein kinase B (Akt)‑related proteins. The results demonstrated that sufentanil had no significant influence on the viability of HCMECs but increased the viability of OGD/R‑induced HCMECs in a dose‑dependent manner. Furthermore, sufentanil inhibited cell apoptosis and permeability of OGD/R‑induced HCMECs but enhanced the protein expression levels of tight junction proteins, including ZO‑1, Occludin, VE‑cadherin and Claudin‑5. Sufentanil was also demonstrated to activate the PI3K/Akt signaling pathway. In addition, the use of LY294002, an inhibitor of the PI3K/Akt signaling pathway, partially abolished the protective effects of sufentanil on apoptosis, permeability and tight junction protein expression levels. These results indicated that sufentanil ameliorated OGD/R‑induced endothelial barrier dysfunction in HCMECs, potentially via the PI3K/Akt signaling pathway. The present study therefore suggested that sufentanil may serve as a novel therapeutic option for the improvement of myocardial I/R injury.
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July-2022
Volume 24 Issue 1

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Spandidos Publications style
Wang L, Ge C and Zhang X: Sufentanil ameliorates oxygen‑glucose deprivation/reoxygenation‑induced endothelial barrier dysfunction in HCMECs via the PI3K/Akt signaling pathway. Exp Ther Med 24: 437, 2022
APA
Wang, L., Ge, C., & Zhang, X. (2022). Sufentanil ameliorates oxygen‑glucose deprivation/reoxygenation‑induced endothelial barrier dysfunction in HCMECs via the PI3K/Akt signaling pathway. Experimental and Therapeutic Medicine, 24, 437. https://doi.org/10.3892/etm.2022.11364
MLA
Wang, L., Ge, C., Zhang, X."Sufentanil ameliorates oxygen‑glucose deprivation/reoxygenation‑induced endothelial barrier dysfunction in HCMECs via the PI3K/Akt signaling pathway". Experimental and Therapeutic Medicine 24.1 (2022): 437.
Chicago
Wang, L., Ge, C., Zhang, X."Sufentanil ameliorates oxygen‑glucose deprivation/reoxygenation‑induced endothelial barrier dysfunction in HCMECs via the PI3K/Akt signaling pathway". Experimental and Therapeutic Medicine 24, no. 1 (2022): 437. https://doi.org/10.3892/etm.2022.11364