Neural stem cells (NSCs) have the potential to give rise to offspring cells and hypoxic injury can impair the function of NSCs. The present study investigated the effects of mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) on NSC injury, as well as the underlying mechanisms. MSC-EVs were isolated and identified via morphological and particle size analysis. Cobalt chloride was used to establish a hypoxic injury model in NSCs. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay was conducted to detect apoptosis. Reverse transcription-quantitative PCR was performed to detect the expression levels of miR- 210-3p, and western blotting was used to detect the expression levels of apoptosis-inducing factor (AI F) and Bcl-2 19 kDa interacting protein (BNI P3). Compared with the control group, NSC apoptosis, and the expression of miR- 210-3p, AI F and BNI P3 were significantly higher in the cobalt chloride-induced hypoxia group. By contrast, treatment with MSC-E Vs further increased miR- 210-3p expression levels, but reduced NSC apoptosis and the expression levels of AI F and BNI P3 compared with the model group (P<0.05). In addition, miR- 210-3p inhibitor reduced miR- 210-3p expression, but promoted hypoxia-induced apoptosis and the expression levels of AI F and BNI P3 compared with the model group (P<0.05). Collectively, the results suggested that MSC-E Vs prevented NSC hypoxia injury by promoting miR- 210-3p expression, which might reduce AI F and BNI P3 expression levels and NSC apoptosis. © 2020 Spandidos Publications. All rights reserved.