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Ischemic brain damage in the role of inflammatory cells
PAGE \* MERGEFORMAT 18
Ischemic brain damage in the role of inflammatory cells
Keywords:: cerebral ischemia pro-inflammatory cytokines
Even immediately after cerebral artery occlusion reperfusion, brain tissue ischemic injury can not be completely back to normal, but can not completely save the brain from secondary injury caused by ischemia and the organization continued to expand [1]. Mechanism of ischemic brain death may be related to the organization acidosis, the release of excitatory amino acid neuronal intracellular calcium accumulation, oxidative stress (protein oxidation, lipid peroxidation, DNA oxidation), nitric oxide synthesis, micro-circulation damage and diffusion suppression and other related depolarization. At present, more research interests focus on ischemia-reperfusion inflammatory process, ischemia-activated endothelial cells and ischemic cells, white blood cells to produce pro-inflammatory cytokines, expression of adhesion molecules, leading to leukocyte accumulation and outflow of [1 ]. Some authors believe that lead to cell death after ischemia may be one of the main factors that infiltration of leukocytes, even suggested one way to treat cerebral ischemia reperfusion artery, the second is to curb the role of pro-inflammatory cytokines [2]. The study now reports are summarized below.
1, cerebral ischemic changes in inflammatory cells
1. The basis of animal experiments: ischemic brain tissue can be seized to CD11 and CD18-positive leukocytes immersion; OX42 immune response to an upward adjustment can be displayed morphological changes associated with activation of microglia and activated microglia cells and immersed in leukocyte surface expression of both ED1, CD68 and major histocompatibility complex (MHC) antigen. And thus the formation of infarcted brain tissue damage associated with endogenous (microglia cells) and exogenous (polymorphonuclear leukocytes, neutrophils, mononuclear cells) inflammatory cell involvement.
Post-infarcti
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