Proinflammatory microglia rely predominantly on glycolysis to maintain cytokine production during ischemia,accompanied with the increases of inducible nitric oxide synthase(iNOS)and monocarboxylate transporter 1(MCT1).Whether there is a link between iNOS and MCT1 expression patterns and pyruvate could act as an energy source to sustain the M1 proinflammatory microglial phenotype,however,remain unclear.In the present study,we examined responses from microglia in the mouse brains subjected to ischemia,and treated with low glucose treatment in vitro.
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