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

Abstract

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 α2-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.

Analgesia in the Neurosurgical Intensive Care Unit

“…The comparable neuroprotective effect was observed with dexmedetomidine in in vitro and in vivo studies. Possible mechanisms are signaling pathways for inflammatory response, oxidative stress, neurotransmitter regulation, mitochondrial function, apoptotic pathway, and autophagy (73). This effect was not confirmed in human studies.…”

Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review

“…It is plausible to consider that the involvement of Ni-induced neuronal injury may be due to exaggerated apoptotic process. Anti-apoptotic agents, which downregulate neuronal caspase 3 expression, are beneficial in NDDs and traumatic brain injury TBI ( Unchiti et al, 2021 ). One cytotoxic study of NiO-NPs against SH-SY5Y determined by caspase-9/3 activity, and expression of apoptotic Bax and Bcl-2 genes assays, demonstrated a significant increase in the mortality of SH-SY5Y cells in an apoptotic fashion suggesting that NiO-NPs may mediate the formation of electrostatic interactions with tau proteins and induction of untoward effects on neurons ( Hajimohammadjafartehrani et al, 2019 , Alquezar et al, 2020 ) examined the neurotoxic effect of nickel in Progressive supranuclear palsy (PSP) cases using two different human cell models.…”

Effect Evaluation of Dexmedetomidine Intravenous Anesthesia on Postoperative Agitation in Patients with Craniocerebral Injury by Magnetic Resonance Imaging Based on Sparse Reconstruction Algorithm

“…At present, the mechanism of postoperative agitation cannot be precisely explained [ 16 , 17 ]. Some scholars believe that the occurrence of postoperative agitation is related to the different degrees of inhibition of the central nervous system by anesthetic drugs [ 11 , 18 ]. Postoperative agitation is a common but difficult complication to be controlled.…”