Role of neuroinflammation in ischemic stroke

Abstract

Ischemic stroke causes the depletion of energy and induce excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Neuroinflammation occurs initially depending on activated resident microglia that has the same function as the macrophage. Activated microglia participates in the neuroinflammatory process by phagocytosing the injured brain cells and producing the pro-and anti-inflammatory mediators. In this review, the authors present an overview of the role of microglia in mediating neuroinflammation in ischemic stroke. Key words:Microglia, ischemic stroke, neuroinflammation ABSTRACT Topic: StrokeThis is an open access article distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

Pathophysiology of Blood–Brain Barrier Permeability Throughout the Different Stages of Ischemic Stroke and Its Implication on Hemorrhagic Transformation and Recovery

“…Other miRNAs can have the capacity of suppressing or promoting the inflammatory response, such as the case of the let-7 family ( 99 ). Ischemia-induced cell death, cell debris, and increased ROS produced in the hyperacute stage lead to neuroinflammation by activating resident microglia and astrocytes ( 100 , 101 ). This activation has been shown to occur 4–6 h after occlusion in animal models of stroke ( 102 ).…”

Peripheral Administration of IL-13 Induces Anti-inflammatory Microglial/Macrophage Responses and Provides Neuroprotection in Ischemic Stroke

“…Despite intensive research during the last decades, ischemic stroke remains a severely dementing and disabling disease with limited options of effective therapy and stands among the major causes of death worldwide. The interruption of cerebral blood flow prompts a cessation of oxygen and nutrients supply, resulting almost instantly in excitotoxicity, oxidative stress, subsequent cellular damage, and apoptosis [1]. Upon the ischemic injury, the primary neuroinflammatory response is initiated by immune cells, such as rapidly activated resident microglia and macrophages, resulting in the local production of inflammatory cytokines and chemokines.…”

Hypertonic saline improves brain edema resulting from traumatic brain injury by suppressing the NF‑κB/IL‑1β signaling pathway and AQP4

“…NF-κB serves as a key player in the neuroinflammatory response in astrocytes during various neurological disorders by promoting the transcription of inflammatory mediators, including proinflammatory cytokines and chemokines (51). IL-1β can be triggered by binding to the receptor IL-1R, which is an upstream signaling factor of NF-κB (52). It has also been demonstrated that IL-1β can increase BBB permeability and disruption by downregulating the expression of TJ proteins (53).…”