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  • Title: Toll-like receptor 4/nuclear factor-kappa B signaling detected in brain after early subarachnoid hemorrhage.
    Author: Ma CX, Yin WN, Cai BW, Wu J, Wang JY, He M, Sun H, Ding JL, You C.
    Journal: Chin Med J (Engl); 2009 Jul 05; 122(13):1575-81. PubMed ID: 19719951.
    Abstract:
    BACKGROUND: Inflammation and immunity play a vital role in the pathogenesis of early brain injury after subarachnoid hemorrhage (SAH). Nuclear factor-kappa B (NF-kappaB) regulates many genes essential for inflammation and immunity and is activated by toll-like receptor (TLR). This study aimed to detect the expression of the toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-kappaB) signaling in the rat brain after early SAH. METHODS: The rats were decapitated and their brains were removed at 0, 2, 4, 6, 12, 24 and 48 hours after a single injection of blood into the prechiasmatic cistern. mRNA expression of TLR4 was measured by Taqman real-time RT-PCR, and protein expression by immunohistochemistry and Western blotting. NF-kappaB activity and concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: TaqMan real-time RT-PCR and Western blotting identified a biphasic change in TLR4 expression in both mRNA and protein: an initial peak (2 - 6 hours) and a sustained elevation (12 - 48 hours). Immunohistochemical staining showed the inducible expression of TLR4-like immunoreactions predominantly in glial cells and vascular endothelium. A similar biphasic change in the activation of NF-kappaB subunit p65 as well as the production of NF-kappaB-regulated proinflammatory cytokines (TNF-alpha, IL-1beta and IL-6) were detected by ELISA. CONCLUSIONS: These data suggest that experimental SAH induces significant up-regulation of TLR4 expression and the NF-kappaB signaling in early brain injury. Activation of the TLR4/NF-kappaB signaling may regulate the inflammatory responses after SAH.
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