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Mediators of Inflammation
Volume 2009, Article ID 473276, 6 pages
http://dx.doi.org/10.1155/2009/473276
Research Article

Activation of TLR4-Mediated NF 𝜅 B Signaling in Hemorrhagic Brain in Rats

1Department of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001, China
2Department of Otorhinolaryngology, The First Affiliated Hospital, China Medical University, Shenyang 110001, China

Received 24 June 2009; Revised 28 August 2009; Accepted 26 October 2009

Academic Editor: Giuseppe Valacchi

Copyright © 2009 Weiyu Teng 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.

Abstract

Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NF 𝜅 B) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NF 𝜅 B signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NF 𝜅 B signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-I 𝜅 B 𝛼 ), and the activity of NF 𝜅 B were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH ( 𝑃 < . 0 5 ). The level of p-I 𝜅 B 𝛼 and the activity of NF 𝜅 B also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NF 𝜅 B signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage.