Pilose antler polypeptide (PAP) is an active substance isolated from the traditional Chinese medicine pilose antler, which possesses multiple biological activities. In the present study, the role and mechanism of PAP in sevoflurane (SEV)‑induced neurocyte injury was explored. Cell viability was determined by Cell Counting kit‑8 assay. Cell proliferation and apoptosis were analyzed by flow cytometry. Western blotting and reverse transcription‑quantitative polymerase chain reaction analysis were used to evaluate the protein and mRNA expression levels, respectively. The results revealed that PAP enhanced the cell viability of SEV‑treated nerve cells. In addition, through modulation of apoptosis‑associated protein expression, PAP suppressed SEV‑induced nerve cell apoptosis. Furthermore, PAP activated the p38 mitogen‑activated protein kinase (p38)/c‑Jun N‑terminal kinase (JNK) pathway in the neurocyte injury model, whereas inhibition of the p38/JNK pathway reversed the beneficial effects produced by PAP. In conclusion, PAP protected against SEV‑mediated neurocyte injury via upregulation of the p38/JNK pathway. The present findings suggested that PAP may be an effective agent for neurocyte injury.