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Schematic mechanism of microglial STING regulates SAH-induced neuroinflammation. SAH insult activated microglial STING. Upon activated, STING phosphorylate, and activate TBK1, which subsequently inhibit the activity of AMPK, resulting microglial activation and polarize into M1 phenotype, accompanied by the secreting of pro-inflammatory mediators and damage to neuron. Pharmacological inhibition of STING with C-176 could attenuate SAH-induced inflammatory injury
