Ischemic brain damage remains the major cause of death and disability worldwide. Bone mesenchymal stem cell (BMSC) transplantation has been identified to serve important roles in cerebral infarction due to its multi?directional differentiation and proliferative ability. However, the function of miR?705 combined with BMSCs on ischemic brain injury remains to be fully elucidated. In the present study, an ischemic brain injury mouse model was constructed, and the mice were injected with BMSCs infected by lentiviral particles expressing miR?705 (BMSCs?Ad?miR?705) to explore the mechanism by which BMSCs?Ad?miR?705 mitigates neurological deficits in ischemic brain damage. In the sham group, no significant neurological injury evaluated via neurological deficit scores was identified, the morphological structure of brain stained with HE was almost normal, and few apoptotic cells were detected by TUNEL assay. However, the PBS group exhibited significant brain damage (P<0.05). BMSCs?Ad (BMSCs infected with control lentiviral particles) and BMSCs?Ad?miR?705 markedly mitigated neurological injury, suppressed morphological damage and inhibited neuronal apoptosis, however promoted the mRNA levels of brain?derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) examined by reverse transcription?quantitative polymerase chain reaction and western blotting. Notably, BMSCs?Ad?miR?705 improved the outcome of BMSCs?Ad transplantation. These data indicated that BMSCs?Ad?miR?705 promoted the secretion of VEGF and BDNF, suppressed neuronal apoptosis, and stimulated neuronal regeneration, in turn mitigating the impairment of ischemic brain damage.

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