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Abstract: Ischemic cerebral stroke is a leading cause of death and long‐term disability world‐wide. Neuronal injury following cerebral ischemia initiates a complex series of signaling cascades that lead to neuronal cell death. MicroRNA 29b (miR‐29b) has reported involvement in the pathogenic process of ischemic brain injury. Dexmedetomidine (Dex) is a highly selective α2 adrenergic receptor stimulant that exerts a protective effect on brain tissue. To determine whether Dex might directly influence miR‐29b expression after an ischemic injury, human neuroblastoma SK‐N‐SH cells were subjected to oxygen‐glucose deprivation (OGD) for the purpose of creating a neuronal injury model that mimics the effects of brain ischemia in vitro. Next, the association of miR‐29b with the protective effect of Dex against ischemic brain injury was studied through the enhancement or inhibition of miR‐29b expression by transfection with an miR‐29b mimic or inhibitor. We demonstrated that Dex treatment could reduce miR‐29b expression, increase cell viability, and inhibit cell apoptosis in the OGD‐induced neuronal injury model in vitro. Furthermore, down‐regulation of miR‐29b expression produced effects on OGD‐induced neuronal injuries that were similar to those produced by Dex treatment. Moreover, up‐regulation of miR‐29b reversed the protective effect of Dex treatment against OGD‐induced neuronal injury. Therefore, down‐regulation of miR‐29b expression might play a role in anti‐apoptotic signaling similar to that played by Dex. Elucidation of the role played by miR‐29b in ischemia, and identification of a definite association between Dex and miR‐29b may lead to the development of new strategies for treating ischemic brain injuries. [ABSTRACT FROM AUTHOR]