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Potential mechanisms of the caffeine treatment-mediated mitigation of hyperoxia-induced lung injury in neonatal mice. High oxygen exposure led to the release of reactive oxygen species (ROS) in newborn mice lung, activated the NF-κB pathway and NLRP3 inflammasomes release, resulted in lung cell damage and alveolar simplification. Caffeine could antagonize A2AR and inhibit the NF-κB pathway, reduce the activation of NLRP3 inflammasome, and alleviate the alveolar injury
