Buyanghuanwu decoction inhibited TLR4-induced activation of nuclear factor-kappa B in acute carbon monoxide poisoning rats

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1 Department of Neurology, Tai Yuan Central Hospital, Taiyuan, China
2 Beijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Beijing, China
3 Department of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan, China
DOI
10.7287/peerj.preprints.1226v1
Published
Accepted
Subject Areas
Immunology, Neurology
Keywords
Acute carbon monoxide poisoning, Buyanghuanwu Decoction, Rat
Copyright
© 2015 Li et al.
Licence
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ PrePrints) and either DOI or URL of the article must be cited.
Cite this article
Li W, Wang X, Guan Z, Zheng Y, Zhang X, Shi J, Niu B. 2015. Buyanghuanwu decoction inhibited TLR4-induced activation of nuclear factor-kappa B in acute carbon monoxide poisoning rats. PeerJ PrePrints 3:e1226v1

Abstract

Acute carbon monoxide poisoning (ACMP) is one of the most common types of poisoning worldwide, and may result in delayed encephalopathy, however, its pathogenesis remains obscure and there is no optimal treatment strategy for the patients with ACMP. Here, we developed the ACMP rat model to observe the protective effects of Buyanghuanwu decoction (BYHWD) on hippocampal neuron. BYHWD (per 5 g/kg) were intragastric administration to rats twice each day for 28 days after ACMP. In ACMP + BYHWD group rats, the neuronal injury in the hippocampal region was significantly less than that of ACMP group’s. BYHWD of intragastric administration also markedly decreased the expression of the TLR4, MyD88, NF-κB P65 after acute carbon monoxide poisoning (P<0.05). TNF-α、IL-1β protein level in ACMP + BYHWD group was lower than that of ACMP group (P<0.05). Our results suggested that decreased the activation of TLR4- NF-κB signal pathway due to BYHWD may partially account for its effect of neuroprotection standing against ACMP, and inhibited the inflammatory reaction to promote the ability recovery of learning and memory in ACMP rats.

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