tlr4在创伤性脑损伤急性炎症损伤中的作用机制及姜黄素的保护效应研究外科学神外专业论文.docxVIP

第三军医大学博士学位论文0PCS 第三军医大学博士学位论文 0PCS 01igodendrocyte precursor cells 少突胶质细胞前体细胞 PFA paraformaldehyde 多聚甲醛 PIP2 phosphatidylinositol一4，5-bisphosphate 4,5-二磷酸磷脂酰肌醇 PRR pattern recognition receptor 模式识别受体 PAMPs pathogen-associated molecular patterns 病原相关分子模式 regulated upon activation normal T-cell调解活化正常T细胞表达和’ ‘4’‘——’ RANTES expressed and secreted 分泌的趋化因子 RIPl receptor-interacting protein 1 受体衔接蛋白1 RT room temperature 室温 TANK TRAF family member associated NFrd3 NFrd3相关TRAF家族激活 activator 蛋白 TAK TGF—p activated kinase TGF．B激酶 TBKl TANK-binding kinase 1 TANK结合激酶 TBI traumatic brain injury 创伤性脑损伤 TLR toll-like receptor Toll样受体 TNF—C【 tumor necrosis factor．c【 肿瘤坏死因子．0【 TNF receptor associated death domain肿瘤坏死因子相关死亡域蛋 ’’一’ TRADD protein 白 TRAF6 tumor necrosis factor receptor-associated肿瘤坏死因子受体相关因子 factor 6 6 TRAM TRIF-related adaptor molecule TRIF相关接头蛋白 TRIF TIR—domain—containing adaptor inducing干扰素TIR结构域衔接蛋白 interferon-p TUNEL transferase mediated deoxyuridine转移酶介导的三磷酸脱氧鸟 triphosphate-biotin nick end labeling 苷．生物素刻痕末端标记 WB westem blot 免疫印迹实验 WT wild type 野生型 2 万方数据 第三军医大学博士学位论文The 第三军医大学博士学位论文 The mechanism of TLR4 in the acute neuroinflammatory lnl ury and tile neUr0DroteCUon ol curcumln alter traumatic brain injury Abstract Traumatic brain injury(TBI)is one common severe disease in neurosurgery with the high incidence in trauma．The mortality and morbidity of TBI are at the head of various types of trauma．In addition to the primary brain injury,the secondary brain inj ury including neural inflammation，free radicals accumulation，excitatory amino acid poisoning， mitochondrial dysfunction and calcium overload Call also damage the brain structure． Studies from animals indicated that the neural inflammation in the acute phase of TBI develops rapidly and lasts for a long time，which play a vital double-edged sword role in the secondary brain injury．The majority of researches suggested that the neural inflammation in acute phase of brain injury is not conducive to survival an