TY - JOUR
A2 - Valacchi, Giuseppe
AU - Teng, Weiyu
AU - Wang, Lishu
AU - Xue, Weishuang
AU - Guan, Chao
PY - 2009
DA - 2010/01/31
TI - Activation of TLR4-Mediated NFB Signaling in Hemorrhagic Brain in Rats
SP - 473276
VL - 2009
AB - Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB 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 NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB 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-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage.
SN - 0962-9351
UR - https://doi.org/10.1155/2009/473276
DO - 10.1155/2009/473276
JF - Mediators of Inflammation
PB - Hindawi Publishing Corporation
KW -
ER -