Activation of TLR4-Mediated NFκB Signaling in Hemorrhagic Brain in Rats. (14th December 2009)

• Record Type: Journal Article
• Authors: Teng, Weiyu; Wang, Lishu; Xue, Weishuang; Guan, Chao
• Other Names: Valacchi Giuseppe Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2009(2009)
• Publication Date: 2009-12-14
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2009/473276
• Languages: English
• ISSNs: 0962-9351

Abstract

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 (NFκ B) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκ 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 NFκ B signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-Iκ Bα ), and the activity of NFκ 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 < .05 ). The level of p-Iκ Bα and the activity of NFκ B also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκ B signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage.