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Research Paper|Volume 14, Issue 24|pp 10153—10170

Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway

Zijun Zhao1,2, Yishuai Li3, Fei Chi4, Li Ma5, Yanan Li1, Zhiyong Hou6, Qiujun Wang1
  • 1Department of Anesthesiology, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, Hebei, China
  • 2Department of Anesthesiology, Hebei Provincial Chest Hospital, Shijiazhuang 050047, Hebei, China
  • 3Department of Thoracic Surgery, Hebei Provincial Chest Hospital, Shijiazhuang 050047, Hebei, China
  • 4Department of Oncology, Hebei Provincial Chest Hospital, Shijiazhuang 050047, Hebei, China
  • 5Surgical Department of Clinical Medicine, Shijiazhuang People’s Medical College, Shijiazhuang 050091, Hebei, China
  • 6Department of Orthopaedics, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, Hebei, China
Received: September 20, 2022Accepted: December 22, 2022Published: December 29, 2022
https://doi.org/10.18632/aging.204461

Copyright: © 2022 Zhao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

To determine whether sevoflurane postconditioning protects against cerebral ischemia reperfusion (I/R) injury and its potential mechanism, we employed bioinformatic analysis, neurological assessments, and western blot analysis, as well as triphenyl tetrazolium chloride, hematoxylin and eosin, Nissl, and immunofluorescence staining. We identified 103 differentially expressed genes induced by cerebral I/R, including 75 upregulated genes and 28 downregulated genes enriched for certain biological processes (involving regulation of inflammatory responses, cellular responses to interleukin 1, and chemokine activity) and signaling pathways (such as transcriptional misregulation in cancer, interleukin-17 signaling, rheumatoid arthritis, MAPK signaling, and Toll-like receptor signaling). As a typical path in Toll-like receptor signaling pathway, in the current study, we investigated the protective effect of sevoflurane postconditioning in cerebral I/R rats and further explore the role of TLR4/MyD88/TRAF6 signaling pathway in it. The results showed cerebral I/R-induced neurological deficits were comparatively less severe following sevoflurane postconditioning. In addition, TLR4/MyD88/TRAF6 signaling pathway-related proteins and neuropathic damage were ameliorated in aged rats following sevoflurane postconditioning, while the TLR4 agonist lipopolysaccharide aggravated these changes. Together, these findings suggest that sevoflurane postconditioning ameliorates cerebral I/R injury by a mechanism involving inhibition of the TLR4/MyD88/TRAF6 signaling pathway to suppress neuroinflammatory responses.