4.6 Article

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

Journal

AGING-US
Volume 14, Issue 24, Pages 10153-10170

Publisher

IMPACT JOURNALS LLC

Keywords

sevoflurane postconditioning; TLR4/MyD88/TRAF6 signaling pathway; cerebral ischemia-reperfusion; neuroinflammation; bioinformatics analysis

Funding

  1. Key project of Natural Science Foundation of Hebei Province [H2021206021]
  2. 2022 Hebei Medical Science Research Project [20221174]

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In this study, we investigated the protective effect of sevoflurane postconditioning against cerebral ischemia reperfusion (I/R) injury and its potential mechanism. The results showed that sevoflurane postconditioning ameliorated neurological deficits induced by cerebral I/R and suppressed neuroinflammatory responses by inhibiting the TLR4/MyD88/TRAF6 signaling pathway.
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.

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