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Objective:   To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells.Methods:   Hydrogen peroxide (H 2 O 2 )-stimulated PC12 cells were divided into control, H 2 O 2 , DEX + H 2 O 2 , miR-NC/inhibitor + H 2 O 2 , and miR-NC/ mimic + DEX + H 2 O 2  groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit.Results:   DEX treatment decreased H 2 O 2 -elevated miR-134 expression. H 2 O 2 -induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H 2 O 2 -induced PC12 cells. However, compared to that in the DEX + H 2 O 2  group, cell viability in the mimic + DEX + H 2 O 2  group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H 2 O 2 -induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H 2 O 2 -induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic.Conclusion:   DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H 2 O 2 -induced PC12 cells by inhibiting the expression of miR-134.

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134