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炎症小体与中枢神经系统疾病

杜秀明 张子腾 宗英 余琛琳 张晓冬 陆国才

杜秀明, 张子腾, 宗英, 余琛琳, 张晓冬, 陆国才. 炎症小体与中枢神经系统疾病[J]. 药学实践与服务, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
引用本文: 杜秀明, 张子腾, 宗英, 余琛琳, 张晓冬, 陆国才. 炎症小体与中枢神经系统疾病[J]. 药学实践与服务, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
DU Xiuming, ZHANG Ziteng, ZONG Ying, YU Chenlin, ZHANG Xiaodong, LU Guocai. Inflammasome and diseases of central nervous system[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
Citation: DU Xiuming, ZHANG Ziteng, ZONG Ying, YU Chenlin, ZHANG Xiaodong, LU Guocai. Inflammasome and diseases of central nervous system[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004

炎症小体与中枢神经系统疾病

doi: 10.3969/j.issn.1006-0111.2016.01.004
基金项目: "重大新药创制"科技重大专项(2014ZX09J14106);国家自然科学基金(81473291、81402651);上海市自然科学基金(13ZR144940);上海市公共卫生重点实验室建设计划(12GWZX0501)

Inflammasome and diseases of central nervous system

  • 摘要: 炎症小体是一蛋白复合物,能够识别不同刺激信号,活化后能诱导免疫和炎症应答。NLRP3炎症小体是中枢神经系统中研究最广泛的炎症小体。小胶质细胞、血管周围的巨噬细胞和脑膜巨噬细胞均能表达炎症小体,而炎症小体与急性脑部感染、急性无菌性脑损伤、帕金森病和阿尔茨海默病等的发生发展有密切关系。基于炎症小体与中枢神经系统疾病相关的机制探索和靶向药物开发是目前的研究热点。
  • [1] de Rivero Vaccari JP,Dietrich WD,Keane RW. Activation and regulation of cellular inflammasomes: gaps in our knowledge for central nervous system injury[J]. J Cereb Blood Flow Metab, 2014, 34(3):369-375.
    [2] Heneka MT, Kummer MP, Andrea Stutz, et al. NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice[J]. Nature, 2013, 493(7434):674-678.
    [3] Weber MD, Frank MG, Tracey KJ, et al. Stress induces the danger-associated molecular pattern HMGB-1 in the hippocampus of male Sprague Dawley rats: a priming stimulus of microglia and the NLRP3 inflammasome[J]. J Neurosci, 2015, 35(1):316-324.
    [4] Ying P, Yang CX, Yu ZQ, et al. Microglial NLRP3 inflammasome activation mediates IL-1β-related inflammation in prefrontal cortex of depressive rats[J]. Brain Behav Immun, 2014, 41:90-100.
    [5] Cribbs DH, Berchtold NC, Perreau V, et al. Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study[J]. J Neuroinflammation, 2012, 9:179-196.
    [6] Shao BZ, Wei W, Ke P, et al. Activating cannabinoid receptor 2 alleviates pathogenesis of experimental autoimmune encephalomyelitis via activation of autophagy and Inhibiting NLRP3 inflammasome[J]. CNS Neurosci Ther, 2014, 20(12):1021-1028.
    [7] Weber MD, Frank MG, Tracey KJ, et al. Stress induces the danger-associated molecular pattern HMGB-1 in the hippocampus of male Sprague Dawley rats: a priming stimulus of microglia and the NLRP3 inflammasome[J]. J Neurosci, 2015, 35:316-324.
    [8] Walsh JG,Muruve DA,Paver C.Inflammasomes in the CNS[J].Nat Rev Neurosci,2014,15(2):84-97.
    [9] Kumar M, Roe K,Orillo B, et al. Inflammasome adaptor protein apoptosis-associated speck-like protein containing CARD (ASC) is critical for the immune response and survival in West Nile virus encephalitis[J]. Virol, 2013, 87:3655-3667.
    [10] Hoegen T, Tremel N,, et al. The NLRP3 inflammasome contributes to brain injury in pneumococcal meningitis and is activated through ATP-dependent lysosomal cathepsin B release[J]. J Immunol, 2011, 187:5440-5451.
    [11] Pradillo JM, Denes A, Greenhalgh AD, et al. Delayed administration of interleukin-1 receptor antagonist reduces ischemic brain damage and inflammation in comorbid rats[J]. J Cereb Blood Flow Metab, 2012, 32:1810-1819.
    [12] Lupfer C, Kanneganti TD. Unsolved Mysteries in NLR Biology[J]. Front Immunol, 2013, 4:285-294.
    [13] Richter K, Kiefer KP, Grzesik BA, et al. Hydrostatic pressure activates ATP-sensitive K+ channels in lung epithelium by ATP release through pannexin and connexin hemichannels[J]. FASEB J, 2014, 28(1):45-55.
    [14] Kampen JMV, Baranowski D, Kay DG. Progranulin gene delivery protects dopaminergic neurons in a mouse model of Parkinson's disease[J]. PLoS One, 2014, 9(5):e97032.
    [15] Codolo G, Plotegher N, Pozzobon T, et al. Triggering of inflammasome by aggregated α-synuclein, an inflammatory response in synucleinopathies[J]. PLoS One,2013,8(1):e55375.
    [16] Lu M, Sun XL, Qiao C, et al. Uncoupling protein 2 deficiency aggravates astrocytic endoplasmic reticulum stress and nod-like receptor protein 3 inflammasome activation[J]. Neurobiology Aging, 2014, 35:421-430.
    [17] Guillot-Sestier MV, Town T. Innate immunity in Alzheimer's disease: a complex affair[J]. CNS Neurol Disord Drug Targets, 2013, 12:593-607.
    [18] Halle A,Hornung V,Petzold GC,et al. The NALP3 inflammassome is involved in the innate immune reponse to amyloid-beta[J].Nat Immunol,2008,9(8):857-865.
    [19] Tan Ms,Yu JT,Jiang T,et al.The NLRP3 inflammasome in Alzheimer's disease[J].Mol Neurobiol,2013,84(3):875-82.
  • [1] 修建平, 杨朝爱, 刘禧澳, 潘乾禹, 韦广旭, 王卫星.  全反式维甲酸对肝星状细胞活化及氧化应激的作用和机制探索 . 药学实践与服务, 2024, 42(7): 1-6. doi: 10.12206/j.issn.2097-2024.202312054
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  • 收稿日期:  2015-07-09
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炎症小体与中枢神经系统疾病

doi: 10.3969/j.issn.1006-0111.2016.01.004
    基金项目:  "重大新药创制"科技重大专项(2014ZX09J14106);国家自然科学基金(81473291、81402651);上海市自然科学基金(13ZR144940);上海市公共卫生重点实验室建设计划(12GWZX0501)

摘要: 炎症小体是一蛋白复合物,能够识别不同刺激信号,活化后能诱导免疫和炎症应答。NLRP3炎症小体是中枢神经系统中研究最广泛的炎症小体。小胶质细胞、血管周围的巨噬细胞和脑膜巨噬细胞均能表达炎症小体,而炎症小体与急性脑部感染、急性无菌性脑损伤、帕金森病和阿尔茨海默病等的发生发展有密切关系。基于炎症小体与中枢神经系统疾病相关的机制探索和靶向药物开发是目前的研究热点。

English Abstract

杜秀明, 张子腾, 宗英, 余琛琳, 张晓冬, 陆国才. 炎症小体与中枢神经系统疾病[J]. 药学实践与服务, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
引用本文: 杜秀明, 张子腾, 宗英, 余琛琳, 张晓冬, 陆国才. 炎症小体与中枢神经系统疾病[J]. 药学实践与服务, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
DU Xiuming, ZHANG Ziteng, ZONG Ying, YU Chenlin, ZHANG Xiaodong, LU Guocai. Inflammasome and diseases of central nervous system[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
Citation: DU Xiuming, ZHANG Ziteng, ZONG Ying, YU Chenlin, ZHANG Xiaodong, LU Guocai. Inflammasome and diseases of central nervous system[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(1): 12-15. doi: 10.3969/j.issn.1006-0111.2016.01.004
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