Inflammation as a therapeutic agent in cerebral infarction: cellular inflammatory response and inflammatory mediators

被引:24
作者
Cuenca-Lopez, Maria D. [1 ]
Brea, David [2 ]
Segura, Tomas
Galindo, Maria F.
Anton-Martinez, David [3 ]
Agulla, Jesus [2 ]
Castillo, Jose [2 ]
Jordan, Joaquin [1 ,4 ]
机构
[1] Univ Castilla La Mancha, Dept Ciencias Med, Fac Med, E-02006 Albacete, Spain
[2] Univ Santiago de Compostela, Hosp Clin Univ, Lab Invest Neurociencias Clin, Serv Neurol, Santiago De Compostela, Spain
[3] Complejo Hosp Univ Albacete, Secc Bioquim, Albacete, Spain
[4] Inst Invest Discapacidades Neurol Albacete, Grp Neurofarmacol, Albacete, Spain
关键词
CNS; Cytokines; Inflammatory mediators; Inflammatory response; Interleukins; Ischaemia; ISCHEMIC BRAIN-INJURY; NECROSIS-FACTOR-ALPHA; CENTRAL-NERVOUS-SYSTEM; NITRIC-OXIDE SYNTHASE; MONOCYTE CHEMOATTRACTANT PROTEIN-1; INTERLEUKIN-1 RECEPTOR ANTAGONIST; TRANSIENT FOCAL ISCHEMIA; RAT-BRAIN; MESSENGER-RNA; TNF-ALPHA;
D O I
10.33588/rn.5006.2009666
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction. The immune central nervous system (CNS) innate immune cells including microglia and macrophages play integral roles in receiving and propagating inflammatory signals. Inflammation is generally a beneficial response of an organism to infection but, when prolonged or inappropriate, it can be detrimental. Neuronal loss in acute (e.g. stroke and head injury) and chronic (e.g. multiple sclerosis and Alzheimer's disease) CNS diseases has been associated with inflammatory processes systemically and in the brain. Development. Herein we review the processes that participate in the activation of the immune system and the starting of inflammatory response after stroke, where neuronal necrotic cell death has been described. We addressed the relevance of the innate inflammatory cells that are on the CNS, as microglia and macrophages, which have an important role in receiving and spreading inflammatory signals. In addition, the inflammatory response is characterized by an increase in the levels of expression of inflammatory mediators, which regulate adhesion molecules, and increase the permeability of the blood-brain barrier. It has also been described that inflammation promotes the rapid over-expression and activation of a variety of genes, and it has been postulated that transcription factors should be studied for their potential use in therapeutics and repair. Transcriptional activation can be a double-edged sword since depending on the individual transcription factor it can induce the expression of either neuroprotective or neurotoxic genes. Conclusion. In summary, a better understanding of the different molecules mediating the immune response will allow the design of new pharmacological tools that could improve stroke treatment.
引用
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页码:349 / 359
页数:11
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