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Hypoxia‑inducible factor‑1α (HIF‑1α) is a key transcriptional factor in response to hypoxia and is involved in ischemic stroke. In the present study, the potential for HIF‑1α to inhibit neuronal apoptosis through upregulating erythropoietin (EPO) was investigated in a transient middle cerebral artery occlusion (tMCAO) rat stroke model. For this purpose, a recombinant adenovirus expressing HIF‑1α was engineered (Ad‑HIF‑1α). Control adenovirus (Ad group), Ad‑HIF‑1α (Ad‑HIF‑1α group) or Ad‑HIF‑1α in addition to erythropoietin mimetic peptide‑9 (EMP9), an EPO‑receptor (‑R) antagonist (Ad‑HIF‑1α+EMP9 group), were used for an intracranial injection into rat ischemic penumbra 1 h following MCAO. All rats demonstrated functional improvement following tMCAO, while the improvement rate was faster in rats treated by Ad‑HIF‑1α compared with all other groups. The EPO‑R inhibitor partially reversed the benefits of Ad‑HIF‑1α. Apoptosis induced by tMCAO was significantly inhibited by Ad‑HIF‑1α (P&lt;0.05). The expression of HIF‑1α, evaluated by immunohistochemistry either in neurons or astrocytes, was upregulated by Ad‑HIF‑1α. Both EPO mRNA and protein expression were increased by Ad‑HIF‑1α, however, there was no significant change of EPO‑R either on an mRNA level or protein level. Furthermore, EMP9 did not change the EPO expression which was upregulated by Ad‑HIF‑1α. Activated caspase 3 in neurons was suppressed by Ad‑HIF‑1α. Activated caspase 3 downregulated by HIF‑1α was partially blocked by EMP9. Altogether, the present data demonstrated that HIF‑1α attenuates neuronal apoptosis partially through upregulating EPO following cerebral ischemia in rat. Thus, upregulating HIF‑1α subsequent to a stroke may be a potential treatment for ischemic stroke.

HIF‑1α attenuates neuronal apoptosis by upregulating EPO expression following cerebral ischemia‑reperfusion injury in a rat MCAO model