Effects of Microglial Activation and Polarization on Brain Injury After Stroke

Abstract

Stroke is one of the most common causes of death worldwide. The subsequent development of neuroinflammation and brain edema dramatically increases the risks associated with stroke, leading to a substantial increase in mortality. Although considerable progress has been made in improving cerebral perfusion in the acute phase of stroke, effective treatment options for the subacute and chronic phases associated with cerebral infarction are limited. Microglia, the innate immune cells of the central nervous system (CNS), can be activated and polarized to take on different phenotypes in response to stimulations associated with stroke, including pro-inflammatory and anti-inflammatory phenotypes, which affect the prognosis of stroke. Therefore, investigation of the activation and polarizing mechanisms of microglia plays a critical role in treating stroke. The aim of this article was to investigate the significance of microglial phenotype regulation in stroke treatment by summarizing the activation, polarizing mechanisms, and general microglia characteristics.

Wild Bitter Melon Extract Abrogates Hypoxia-Induced Cell Death via the Regulation of Ferroptosis, ER Stress, and Apoptosis in Microglial BV2 Cells

“…Microglial cells are activated under ischemia and polarize into proinflammatory (M1) and anti-inflammatory (M2) phenotypes in response to stimulation associated with stroke [3]. Qin and Crews reported that activated M1-type microglia promote reactive oxygen species (ROS) overproduction via NADPH oxidase upregulation, increase the production of proinflammatory factors, and finally cause neuronal damage [4].…”

“…Microglial cells have also been considered the principal immune cells in the brain and are the first line of defense against the pathophysiology induced by stroke, which causes a large number of families worldwide to suffer from physical and mental burden [ 2 ]. Microglial cells are activated under ischemia and polarize into proinflammatory (M1) and anti-inflammatory (M2) phenotypes in response to stimulation associated with stroke [ 3 ]. Qin and Crews reported that activated M1-type microglia promote reactive oxygen species (ROS) overproduction via NADPH oxidase upregulation, increase the production of proinflammatory factors, and finally cause neuronal damage [ 4 ].…”

Impact of Fetal Growth Restriction on the Neonatal Microglial Proteome in the Rat

“…Microglia can acquire distinct phenotypes in response to perinatal inflammatory events, not only contributing to the restoration of brain homeostasis but also supporting repair and regulating important physiological processes, including synaptic pruning [11][12][13][14][15][16]. Response to injury in the developing brain is usually associated with but not restricted to an inflammatory response of microglia [17].…”

Underlying Mechanism and Active Ingredients of Tianma Gouteng Acting on Cerebral Infarction as Determined via Network Pharmacology Analysis Combined With Experimental Validation

“…Inflammatory responses are involved in all stages of stroke-related injury, including early cerebral-infarction tissue repair and regeneration after ischemia ( Ghelani Drishti et al, 2021 ) and neuroinflammation that alters neuronal structure and function ( Mehta et al, 2017 ). Microglial, innate immune cells of the CNS can be activated and polarized to assume various phenotypes in response to stroke-induced stimulatory signals to greatly influence stroke prognosis ( Dong et al, 2021 ). Following CI, microglial activation occurs that leads to significantly increased aggregation of inflammatory cells and secretion of cytokines, with concurrent induction of acute neuroinflammation triggered by neuronal hypoxia within brain tissues.…”