Intracerebral hemorrhage (ICH) is a disease associated with high mortality and morbidity. MicroRNAs (miRNAs) are important regulators of translation and have been reported to be associated with the pathogenesis of numerous cerebrovascular diseases, including ICH. The present study explored the role of miRNA (miR)‑126 in ICH. Adult male Wistar rats were randomly assigned to ICH model and sham groups. ICH was induced by intracerebral injection of collagenase. The mRNA expression levels of miR‑126 in the two groups were determined. The miR‑126 lentivirus expression vector pWPXL‑miR‑126 or negative control vector was then constructed and delivered via intraparenchymal injection. Following transduction, behavioral testing (rotarod and limb placement tests), relative hemorrhagic lesion size, apoptotic cells and protein levels of vascular endothelial growth factor (VEGF)‑A and caspase‑3 were determined. The relative expression levels of miR‑126 were significantly decreased in the ICH group compared to the sham group (P=0.026). Overexpression of miR‑126 significantly improved the relative duration of stay on the rotarod at day 2 (P=0.029) and 3 (P=0.033), and statistically reduced the deficit score (P=0.036), the relative size of hemorrhagic lesion (P=0.019) and the number of apoptotic cortical neurons (P=0.024) compared with the sham group. Additionally, the protein levels of VEGF‑A were significantly elevated, however levels of caspase‑3 were downregulated by overexpression of miR‑126 compared with the negative control group. MiR‑126 therefore exhibits a protective role in ICH. Overexpression of miR‑126 protects against ICH, and may be involved in the process of angiogenesis and exhibit an anti-apoptotic effect.