Microglia are immune cells in the brain that can respond to endogenous and exogenous substrates to elicit inflammatory reactions. The transcription factor nuclear factor kappa-light-chain-enhancer of activated B induces proinflammatory gene expression in response to foreign matter via pattern recognition receptors; thus, nuclear factor kappa-light-chain-enhancer of activated B is a master regulator of inflammation. During the inflammatory process, very large amounts of reactive oxygen species are generated and promote the onset and progression of inflammation. Interestingly, nuclear factor kappa-light-chain-enhancer of activated B drives the transcription of superoxide dismutase 2 in many types of cells, including microglia. Superoxide dismutase 2 is an antioxidative enzyme that catalyzes the dismutation of superoxide anions into molecular oxygen and hydrogen peroxide. Of note, nuclear factor kappa-light-chain-enhancer of activated B can initiate inflammation to elicit proinflammatory gene expression, while its transcription product superoxide dismutase 2 can suppress inflammation. In this review, we use recent knowledge to describe the interaction between oxidative stress and nuclear factor kappa-light-chain-enhancer of activated B and discuss the complicated role of microglial superoxide dismutase 2 in inflammation.
Keywords: NF-κB; inflammation; microglia; reactive oxygen species; superoxide dismutase 2.
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