Peer-reviewedCC BY-NC-ND 4.0In Vivo29 Oct 2026

Urolithin A Attenuates Noise-induced Hearing Loss and Is Associated With Increased Cochlear Mitophagy Markers

SUNG IL CHO^1,2
EU-RI JO^1,3
JEONGHYUN OH¹

¹Department of Otolaryngology-Head and Neck Surgery, Chosun University College of Medicine, Gwangju, Republic of Korea
²Medical Research Institute, Chosun University, Gwangju, Republic of Korea
³Department of Biomedical Sciences, Graduate School of Chosun University, Gwangju, Republic of Korea

Abstract

Background/Aim: Noise-induced hearing loss (NIHL) is a prevalent cause of sensorineural hearing impairment, in which mitochondrial dysfunction plays a key pathogenic role. Mitophagy is essential for maintaining mitochondrial quality control. This study investigated whether urolithin A (UA), a known mitophagy inducer, protects against NIHL.

Materials and Methods: Eight-week-old CBA/J mice were divided into three groups: control, noise + saline, and noise + UA (10 mg/kg). NIHL was induced by exposure to broadband noise (100 dB SPL, 2 h). UA was administered intraperitoneally before and after noise exposure. Auditory function was evaluated using auditory brainstem response (ABR). Mitophagy-associated markers and mitochondrial function were assessed by Western blotting, quantitative real-time PCR, mitochondrial DNA (mtDNA) integrity analysis, ATP measurements, and immunohistochemistry/immunofluorescence.

Results: UA treatment significantly reduced auditory threshold shifts compared with the untreated group. The expression levels of mitophagy-related proteins and genes, including PINK1, Parkin, and BNIP3, were significantly increased in the UA-treated group. In addition, UA restored ATP levels following noise exposure. Immunohistochemical and immunofluorescence analyses demonstrated enhanced formation of mitophagosomes and mitophagolysosomes in the cochlea, including the organ of Corti and the spiral ganglion, in the UA-treated group.

Conclusion: UA attenuates NIHL by enhancing mitophagy-associated markers and preserving mitochondrial function in the cochlea. These findings suggest that pharmacological activation of mitophagy may represent a promising therapeutic strategy for NIHL.

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BibTeX RIS

BibTeX

@article{il2026urolithin,
  title = {{Urolithin A Attenuates Noise-induced Hearing Loss and Is Associated With Increased Cochlear Mitophagy Markers}},
  author = {SUNG IL CHO and EU-RI JO and JEONGHYUN OH},
  journal = {In Vivo},
  year = {2026},
  month = oct,
  doi = {10.21873/invivo.14481},
  url = {https://doi.org/10.21873/invivo.14481},
  note = {CC BY-NC-ND 4.0},
}

RIS

TY  - JOUR
TI  - Urolithin A Attenuates Noise-induced Hearing Loss and Is Associated With Increased Cochlear Mitophagy Markers
AU  - SUNG IL CHO
AU  - EU-RI JO
AU  - JEONGHYUN OH
PY  - 2026
DA  - 2026/10/29
JO  - In Vivo
DO  - 10.21873/invivo.14481
UR  - https://doi.org/10.21873/invivo.14481
AB  - Background/Aim: Noise-induced hearing loss (NIHL) is a prevalent cause of sensorineural hearing impairment, in which mitochondrial dysfunction plays a key pathogenic role. Mitophagy is essential for maintaining mitochondrial quality control. This study investigated whether urolithin A (UA), a known mitophagy inducer, protects against NIHL.  Materials and Methods: Eight-week-old CBA/J mice were divided into three groups: control, noise + saline, and noise + UA (10 mg/kg). NIHL was induced by exposure to broadband noise (100 dB SPL, 2 h). UA was administered intraperitoneally before and after noise exposure. Auditory function was evaluated using auditory brainstem response (ABR). Mitophagy-associated markers and mitochondrial function were assessed by Western blotting, quantitative real-time PCR, mitochondrial DNA (mtDNA) integrity analysis, ATP measurements, and immunohistochemistry/immunofluorescence.  Results: UA treatment significantly reduced auditory threshold shifts compared with the untreated group. The expression levels of mitophagy-related proteins and genes, including PINK1, Parkin, and BNIP3, were significantly increased in the UA-treated group. In addition, UA restored ATP levels following noise exposure. Immunohistochemical and immunofluorescence analyses demonstrated enhanced formation of mitophagosomes and mitophagolysosomes in the cochlea, including the organ of Corti and the spiral ganglion, in the UA-treated group.  Conclusion: UA attenuates NIHL by enhancing mitophagy-associated markers and preserving mitochondrial function in the cochlea. These findings suggest that pharmacological activation of mitophagy may represent a promising therapeutic strategy for NIHL.
SN  - 0258-851X
SN  - 1791-7549
ER  -

Abstract

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