ArticleMolecular medicine reports2018
Pilose antler polypeptide protects against sevoflurane‑mediated neurocyte injury.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Genetic Assessment of Neurotoxicity Accompanied by Inhalational Anesthesia in Preclinical Studies with Focus on Sevoflurane and Isoflurane-A Narrative Review.Brain sciences · 2026Review
- Deer antler polypeptides promote osteogenesis for fracture healing via activating neurosensory PGE2/EP4/p-CREB axis.Journal of orthopaedic translation · 2026Article
- Well-known polypeptides of deer antler velvet with key actives: modern pharmacological advances.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Health Effects of Peptides Extracted from Deer Antler.Nutrients · 2022Review
- The Protective Effect of Pilose Antler Peptide on CUMS-Induced Depression Through AMPK/Sirt1/NF-κB/NLRP3-Mediated Pyroptosis.Frontiers in pharmacology · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
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.
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