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BioMed Research International
Volume 2017 (2017), Article ID 4286738, 9 pages
Research Article

Effects of TLR3 and TLR9 Signaling Pathway on Brain Protection in Rats Undergoing Sevoflurane Pretreatment during Cardiopulmonary Bypass

1Department of Anesthesiology, General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning 110016, China
2Department of Laboratory Animal Science, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China

Correspondence should be addressed to Zhang Tiezheng and Chen Keyan

Received 4 June 2017; Revised 22 October 2017; Accepted 7 November 2017; Published 27 December 2017

Academic Editor: Alfredo Conti

Copyright © 2017 Zhou Nan et al. 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.


Objective. To investigate the effects of TLR3 and TLR9 signaling pathway on brain injury during CPB in rats pretreated with sevoflurane and its possible molecular mechanism. Methods. SD rats were randomly assigned to sham group, CPB group, and Sev group. Brain tissue was obtained at before CPB (), at CPB for 30 minutes (), 1 hour after CPB (), and 3 hours after CPB (). ELISA was used to measure S100-β and IL-6. Western blot was utilized to determine TLR3 and TLR9 expression. TUNEL was applied to detect neuronal apoptosis. Results. Compared with CPB group, at , at termination after 1 hour of CPB (), , 2 hours after CPB () and , S100-β and IL-6 decreased in Sev group. Compared with CPB group, IFN-β were increased in Sev group, except . Compared with CPB group, TLR3 expression increased, and TLR9 and NF-κB decreased in Sev group. The apoptotic neurons were less in Sev group than in CPB group (). Conclusion. Sevoflurane intervention can activate TLR3 and TLR9 signaling pathway, upregulate TLR3 expression and downstream TRIF expression, decrease TLR9 expression, and downregulate downstream NF-κB expression in CPB rat models, thereby mitigating brain injury induced by inflammatory response during CPB.