The potential role of dexmedetomidine on neuroprotection and its possible mechanisms: Evidence from in vitro and in vivo studies

Neurological disorders following brain injuries and neurodegeneration are on the rise worldwide and cause disability and suffering in patients. It is crucial to explore novel neuroprotectants. Dexmedetomidine, a selective alpha 2-adrenoceptor agonist, is commonly used for anxiolysis, sedation and analgesia in clinical anaesthesia and critical care. Recent studies have shown that dexmedetomidine exerts protective effects on multiple organs. This review summarized and discussed the current neuroprotective effects of dexmedetomidine, as well as the underlying mechanisms. In preclinical studies, dexmedetomidine reduced neuronal injury and improved functional outcomes in several models, including hypoxia-induced neuronal injury, ischaemic-reperfusion injury, intracerebral haemorrhage, post-traumatic brain injury, anaesthetic-induced neuronal injury, substance-induced neuronal injury, neuroinflammation, epilepsy and neurodegeneration. Several mechanisms are associated with the neuroprotective function of dexmedetomidine, including neurotransmitter regulation, inflammatory response, oxidative stress, apoptotic pathway, autophagy, mitochondrial function and other cell signalling pathways. In summary, dexmedetomidine has the potential to be a novel neuroprotective agent for a wide range of neurological disorders.

Automated summary

Dexmedetomidine, a selective alpha 2-adrenoceptor agonist, has shown neuroprotective effects in various models of neuronal injury. Its mechanisms of neuroprotection involve neurotransmitter regulation, inflammatory response, oxidative stress, and other cell signalling pathways. Dexmedetomidine holds promise as a novel neuroprotective agent for a wide range of neurological disorders.