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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Neuroinflammation: friend and foe for ischemic stroke

Fig. 2

Schematic representation of post-ischemic inflammatory response in stroke. Initial ischemic event leads to oxidative stress and excitotoxicity which causes activation of microglia and astrocyte resulting in secretion of cytokines, MMP, and GFAP. These proinflammatory factors leads to upregulation of cell adhesion molecules such as ICAM-1 and selectins on endothelial cells causing inflow of blood derived inflammatory cells such as neutrophils, macrophages, and lymphocytes to the ischemic area. In addition, danger-associated molecular patterns (DAMPs) are released by dying neurons that in turn activates microglia and peripheral immune cells (neutrophil, macrophage, and lymphocyte) resulting in production of proinflammatory factors causing further activation of microglia and astrocyte. These pathological events lead to neuronal death and further increase damage to the ischemic brain

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