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Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR‑29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4 (AQP4). Real‑time PCR and western blotting were used to assess miR‑29a levels and AQP4 protein levels, respectively. Apoptosis was detected by flow cytometry, and lactate dehydrogenase (LDH) was determined by enzyme‑linked immunosorbent assay (ELISA). Overexpression of miR‑29a was significantly downregulated in OGD‑induced primary astrocytes, and transfection with a miR‑29a mimic decreased LDH release and apoptosis, and improved cell health in OGD‑induced astrocytes. AQP4 was the target of miR‑29a, which suppressed AQP4 expression, and knockdown of AQP4 mitigated OGD‑induced astrocyte injury. Furthermore, miR‑29a regulated AQP4 expression in OGD‑induced astrocytes. AQP4 exacerbated astrocyte injury following ischemic stroke, and knockdown of AQP4 protected OGD/RX‑induced primary cultured astrocytes against injury. The effect of miR‑29a inhibitor on primary astrocytes was lost following AQP4 knockdown. These findings indicated that miR‑29a prevented astrocyte injury in vitro by inhibiting AQP4. Thus, miR‑29a may protect primary cultured astrocytes after OGD‑induced injury by targeting AQP4, and may be a potential therapeutic target for ischemic injury of astrocytes.

miR‑29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4