MiR-206 is involved in neuroprotective effects of Dexmedetomidine in H₂O₂-induced SK-N-SH cells by targeting ANXA1

Abstract

This study focused on exploring the neuroprotective role of Dexmedetomidine (DEX) and miR-206 in H₂O₂-induced SK-N-SH cells. First, we dectected the cell viability, apotosis, oxidative stress and miR-206 expression in H₂O₂-treated SK-N-SH cells.Next, we examined above content in H₂O₂-induced SK-N-SH cells though DEX treatment. Besides, the level of cell viability, apotosis, oxidative stress were evaluated in H₂O₂-treated SK-N-SH cells transfected with miR-206 mimics and miR-206 inhibitor. Moreover, the target gene of miR-206 were predicted and verifed by binformatics tools and luciferase reporter assay. These data indicated that H₂O₂ evoked the apotosis, oxidative stress and inhibition of miR-206 expression in SK-N-SH cells in a dose manner. Besides, DEX attenuated H₂O₂-induced oxidative damage, apotosis and promoted miR-206 expression in SK-N-SH cells. Moreover, overexpression of miR-206 augmented the cell viablity as well as suppressed apotosis and oxidative stress in H₂O₂-induced SK-N-SH cells, while down-expression of miR-206 showed opppsite effects. Further, Annexin A1 (ANXA1) was verified as a directly target of miR-206, and over-expression of ANXA1 could slack the neuroprotective effect of miR-206 in H₂O₂-induced SK-N-SH cells. DEX exerted neuroprotective effects on H₂O₂-treated SK-N-SH cells in vitro by negatively reguating ANXA1 expression via activation of miR-206.

Keywords:
dexmedetomidine; miR-206; annexin A1; hypoxic–ischaemic brain damage