ArticleeNeuro
Agmatine Alleviates Cisplatin-Induced Ototoxicity by Activating PI3K/AKT Signaling Pathway.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Agmatine Sulfate Is Associated with Altered Redox Status, Apoptosis-Associated Responses, and AKT/JNK Signalling in Ishikawa Endometrial Cancer Cells.Life (Basel, Switzerland) · 2026Article
- Multitarget protection by Chinese herbal medicines against sensorineural hearing loss: a focus on oxidative stress, apoptosis, and inflammation.Frontiers in medicine · 2026Review
- Taurine Alleviates Inflammation, Oxidative Stress, Apoptosis, and Uterus Microbiota Dysregulation of Endometritis by Inhibiting PI3K-AKT/MAPK/NF-κB Pathways in Mice.Animals : an open access journal from MDPI · 2025Article
- From Ototoxicity to Otoprotection: Mechanism and Protective Strategies in Cisplatin Therapy.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Acquired sensorineural hearing loss, oxidative stress, and microRNAs.Neural regeneration research · 2025Article
- Crosslinked-hybrid nanoparticle embedded in thermogel for sustained co-delivery to inner ear.Journal of nanobiotechnology · 2024Article
- Stress granules formation in HEI-OC1 auditory cells and in H4 human neuroglioma cells secondary to cisplatin exposure.Cell stress · 2024Article
- Cisplatin ototoxicity mechanism and antagonistic intervention strategy: a scope review.Frontiers in cellular neuroscience · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin-induced ototoxicity can be partially attributed to excessive reactive oxygen species (ROS) production, and agmatine is well-known for the activation of the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) pathway to inhibit ROS production. Whether agmatine could be used to alleviate cisplatin-induced ototoxicity is investigated. Cisplatin-exposed House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and cochlear explants showed increased ROS production detected by 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) staining and decreased cell viability detected by Cell Counting Kit-8 (CCK-8) or Myosin 7a staining, which could be reversed by the agmatine pretreatment. Cisplatin intraperitoneally injected C57BL/6 mice demonstrated damaged auditory function as indicated by distortion products otoacoustic emissions (DPOAEs) and auditory brainstem response (ABR) assays, and trans-tympanically administrated agmatine in the left ears could partly prevent the auditory function loss. Mechanistically, downregulated B-cell lymphoma 2 (Bcl-2) expression, upregulated Bcl2-associated x (Bax) expression, and diminished p-PI3K and p-AKT expression were detected in cisplatin-exposed HEI-OC1 cells and cochlear explants, which could be prevented by the pretreatment with agmatine. Our investigation demonstrates that agmatine pretreatment could alleviate cisplatin-induced ototoxicity with the activation of PI3K/AKT signaling pathway.
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