Activation of microglia induces the production of many mediators that mediate the different pathological processes of stroke. Due to the diversity of mediators, they also exert different effects on different pathological processes in the stroke process. A clinical study on stroke found that, on the one hand, activated microglia in the infarct zone can exacerbate delayed neuronal death by producing toxic substances. On the other hand, activated microglia promote neuronal regeneration by producing growth factors. However, it is not clear about the specific role of microglia in stroke. Therefore, Ace Therapeutics provides comprehensive services to explore the role of microglia in stroke pathology from different perspectives by combining current studies.
Many factors have the ability to activate microglia, such as Toll-like receptors, histamine and substance P, and programmed cell death protein 1. In contrast, activated microglia disrupt blood-brain barrier permeability and enhance apoptosis of astrocytes. Ace Therapeutics provides comprehensive services to detect the effects of activated microglia on the stroke process.
In response to stimulation by anti-inflammatory and pro-inflammatory factors, microglia can generally polarize into inflammatory phenotype (M1 phenotype) and anti-inflammatory phenotype (M2 phenotype). M1 phenotype produces a variety of pro-inflammatory factors such as IL-1β, IL-6, TNF-α, CCL2, CXCL10, and others. It is generally believed that the M1 phenotype promotes inflammatory responses while the M2 phenotype has protective effects. Ace Therapeutics provides a comprehensive service to explore the role of different phenotypes of microglia in the stroke process.
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