Dexmedetomidine (DEX), an α2 adrenoceptor agonist, is a commonly used anesthetic drug in surgical procedures. Previous studies have indicated that DEX exerts neuroprotective effects. However, the molecular mechanism underlying this process remains to be elucidated. The present study investigated a potential implication of microRNA (miR)‑223‑3p in the DEX‑induced anti‑oxidative effect on neuronal cells. The results indicated that following hydrogen peroxide (H2O2)‑mediated induction of oxidative stress, the viability of human hippocampal neuronal cells was markedly decreased, as determined by an MTT assay. In addition, treatment with H2O2 induced cell apoptosis, the release of lactate dehydrogenase, accumulation of intracellular calcium, phosphorylation of calmodulin‑2, and production of malondialdehyde and reactive oxygen species. Furthermore, treatment with H2O2 inhibited the expression of mir‑223‑3p and enhanced the expression of its target cytotoxic granule associated RNA binding protein like 1 (TIAL1), and these effects were reversed by treatment with DEX. Mechanistic studies demonstrated that the 3'‑untranslated region of TIAL1 is a direct target of mir‑223‑3p. The results of the present study demonstrated that DEX may induce its neuroprotective effects by regulating the interaction between miR‑223‑3p and TIAL1. Therefore, the manipulation of miR‑223‑3p/TIAL1 interaction may be involved in the neuroprotective effects of DEX.
Keywords: exmedetomidine; oxidative stress; microRNA-223-3p; TIA1 cytotoxic granule-associated RNA binding protein-like 1; neuronal cells.