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Int. J. Mol. Sci. 2017, 18(11), 2347; https://doi.org/10.3390/ijms18112347

Sevoflurane Postconditioning-Induced Anti-Inflammation via Inhibition of the Toll-Like Receptor-4/Nuclear Factor Kappa B Pathway Contributes to Neuroprotection against Transient Global Cerebral Ischemia in Rats

1
Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam 13620, Korea
2
Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul 03080, Korea
*
Author to whom correspondence should be addressed.
Received: 14 September 2017 / Revised: 12 October 2017 / Accepted: 26 October 2017 / Published: 6 November 2017
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Abstract

The anti-inflammatory actions of sevoflurane postconditioning are suggested as an important mechanism of sevoflurane postconditioning-induced neuroprotection against cerebral ischemia. Here, we determined whether the anti-inflammatory effects of sevoflurane postconditioning were mediated via inhibition of the toll-like receptor (TLR)-4/nuclear factor kappa B (NF-κB) pathway after global transient cerebral ischemia in rats. Forty-five rats were randomly assigned to five groups as follows: (1) control (10 min of ischemia, n = 10); (2) sevoflurane postconditioning (two periods of sevoflurane inhalation after ischemia for 10 min with a wash period of 10 min, n = 10); (3) resatorvid (intraperitoneal injection of a selective TLR-4 antagonist (3 mg/kg) 30 min before ischemia, n = 10); (4) sevoflurane postconditioning plus resatorvid (n = 10), and sham (n = 5). The numbers of necrotic and apoptotic cells in the hippocampal CA1 region, the expression levels of TLR-4, NF-κB, cleaved caspase-3, and tumor necrosis factor alpha (TNF-α) in the anterior part of each brain, and the serum levels of TNF-α, interleukin 6 (IL-6), and interleukin 1 beta (IL-1β) were assessed 1 day after ischemia. The necrotic cell counts and expression levels of TLR-4, NF-κB, caspase-3, and TNF-α in brain tissue as well as serum levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) were significantly higher in the control group than in the other groups. Our findings suggest that the anti-inflammatory actions of sevoflurane postconditioning via inactivation of the TLR-4/NF-κB pathway and subsequent reduction in pro-inflammatory cytokine production, in part, contribute to sevoflurane postconditioning-induced neuroprotection after global transient cerebral ischemia in rats. View Full-Text
Keywords: inflammation; sevoflurane postconditioning; neuroprotection inflammation; sevoflurane postconditioning; neuroprotection
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Hwang, J.-W.; Jeon, Y.-T.; Lim, Y.-J.; Park, H.-P. Sevoflurane Postconditioning-Induced Anti-Inflammation via Inhibition of the Toll-Like Receptor-4/Nuclear Factor Kappa B Pathway Contributes to Neuroprotection against Transient Global Cerebral Ischemia in Rats. Int. J. Mol. Sci. 2017, 18, 2347.

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