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Li S, Xu J, Yao W, et al. Sevoflurane pretreatment attenuates TNF-α-induced human endothelial cell dysfunction through activating eNOS/NO pathway. Biochem Biophys Res Commun. 2015;460(3):879-86doi: 10.1016/j.bbrc.2015.03.126.
Li, S., Xu, J., Yao, W., Li, H., Liu, Q., Xiao, F., Irwin, M. G., Xia, Z., & Ruan, W. (2015). Sevoflurane pretreatment attenuates TNF-α-induced human endothelial cell dysfunction through activating eNOS/NO pathway. Biochemical and biophysical research communications, 460(3), 879-86. https://doi.org/10.1016/j.bbrc.2015.03.126
Li, Suobei, et al. "Sevoflurane pretreatment attenuates TNF-α-induced human endothelial cell dysfunction through activating eNOS/NO pathway." Biochemical and biophysical research communications vol. 460,3 (2015): 879-86. doi: https://doi.org/10.1016/j.bbrc.2015.03.126
Li S, Xu J, Yao W, Li H, Liu Q, Xiao F, Irwin MG, Xia Z, Ruan W. Sevoflurane pretreatment attenuates TNF-α-induced human endothelial cell dysfunction through activating eNOS/NO pathway. Biochem Biophys Res Commun. 2015 May 08;460(3):879-86. doi: 10.1016/j.bbrc.2015.03.126. Epub 2015 Mar 31. PMID: 25838201.
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Biochem Biophys Res Commun. 2015 May 08;460(3):879-86. doi: 10.1016/j.bbrc.2015.03.126. Epub 2015 Mar 31.

Sevoflurane pretreatment attenuates TNF-α-induced human endothelial cell dysfunction through activating eNOS/NO pathway.

Biochemical and biophysical research communications

Suobei Li, Junmei Xu, Weifeng Yao, Haobo Li, Qing Liu, Feng Xiao, Michael G Irwin, Zhengyuan Xia, Wei Ruan

Affiliations

  1. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Anesthesia Research Institute, Central South University, Changsha, Hunan, China.
  2. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Anesthesia Research Institute, Central South University, Changsha, Hunan, China. Electronic address: [email protected].
  3. Department of Anesthesiology, University of Hong Kong, Hong Kong, China.
  4. Department of Anesthesiology, University of Hong Kong, Hong Kong, China; Department of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.
  5. Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Anesthesia Research Institute, Central South University, Changsha, Hunan, China. Electronic address: [email protected].

PMID: 25838201 DOI: 10.1016/j.bbrc.2015.03.126

Abstract

Endothelial dysfunction induced by oxidative stress and inflammation plays a critical role in the pathogenesis of cardiovascular diseases. The anesthetic sevoflurane confers cytoprotective effects through its anti-inflammatory properties in various pathologies such as systemic inflammatory response syndrome and ischemic-reperfusion injury but mechanism is unclear. We hypothesized that sevoflurane can protect against tumor necrosis factor (TNF)-α-induced endothelial dysfunction through promoting the production of endothelium-dependent nitric oxide (NO). Primary cultured human umbilical vein endothelial cells (HUVECs) were pretreated with different concentrations (0.5, 1.5 and 2.5 minimum alveolar concentration, MAC) of sevoflurane for 30 min before TNF-α (10 ng/mL) stimulation for 4 h. Sevoflurane pretreatment significantly reduced TNF-α-induced VCAM-1, ICAM-1, IκBα, and NF-κB activation, and blocked leukocytes adhesion to HUVECs. Meanwhile, sevoflurane (1.5 and 2.5 MAC) significantly induced endothelial nitric oxide synthase (eNOS) phosphorylation and enhanced NO levels both intracellularly and in the cell culture medium. All these cytoprotective effects of sevoflurane were abrogated by NG-nitro-l-arginine methyl ester (l-NAME), a non-specific nitric oxide synthase inhibitor. Collectively, these data indicate that sevoflurane protects against TNF-α -induced vascular endothelium dysfunction through activation of eNOS/NO pathway and inhibition of NF-κB.

Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

Keywords: Endothelial nitric oxide synthase; Human umbilical vein endothelial cells; Inflammation; Sevoflurane

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