ArticleScientific reports2025
Protective effects of indole-3-propionic acid against TCP-induced hearing loss in mice by mitigating oxidative stress and promoting neutrophil recruitment.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Review
- Microbiota-Derived Tryptophan Metabolite Indole-3-Propionic Acid-Emerging Role in Neuroprotection.Molecules (Basel, Switzerland) · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Sensorineural hearing loss (SNHL) poses a significant global health challenge with substantial socioeconomic and medical implications. The pathophysiology involves excessive reactive oxygen species (ROS) in the cochlea, inflammation, cellular apoptosis, etc. Tryptophan metabolite indole-3-propionic Acid (IPA), produced by gut microbiota, may offer therapeutic benefits by modulating inflammation, oxidative stress, and immune responses. However, the roles of IPA in protecting from treatment hearing loss in adult mice remain to be investigated. We previously validated that exposure to pesticide metabolite 3, 5, 6-Trichloro-2-pyridinol (TCP) caused hearing loss in mice. Herein, continuous administration of 40 mg/kg IPA for 21 days significantly attenuated the hearing threshold elevation in C57BL/6 mice exposed to 50 mg/kg TCP. IPA treatment reduced the loss of hair cells (HCs) and spiral ganglion neurons (SGNs), preserved nerve fibers, and reversed the damage to spiral ligaments (SL) and stria vascularis (SV). Similarly, IPA cotreatment decreased ROS accumulation in the cochlea and inhibited HC and SGN apoptosis. Transcriptomic analysis showed that IPA enhanced immune responses, particularly through neutrophil recruitment and the activation of regenerative signals like IFNγ. These findings underscore IPA's protective effects against TCP-induced hearing loss, highlighting the role of immune mechanisms in cochlear protection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.