Noise-induced cochlear damage involves ppar down-regulation through the interplay between oxidative stress and inflammation

Fabiola Paciello, Anna Pisani, Rolando Rolesi, Vincent Escarrat, Jacopo Galli, Gaetano Paludetti, Claudio Grassi*, Diana Troiani, Anna Rita Fetoni*

*Autore corrispondente per questo lavoro

Risultato della ricerca: Contributo in rivistaArticolo in rivistapeer review


The cross-talk between oxidative stress and inflammation seems to play a key role in noise-induced hearing loss. Several studies have addressed the role of PPAR receptors in mediating antioxidant and anti-inflammatory effects and, although its protective activity has been demonstrated in several tissues, less is known about how PPARs could be involved in cochlear dysfunction induced by noise exposure. In this study, we used an in vivo model of noise-induced hearing loss to investigate how oxidative stress and inflammation participate in cochlear dysfunction through PPAR signaling pathways. Specifically, we found a progressive decrease in PPAR expression in the cochlea after acoustic trauma, paralleled by an increase in oxidative stress and inflammation. By comparing an antioxidant (Q-ter) and an anti-inflammatory (Anakinra) treatment, we demonstrated that oxidative stress is the primary element of damage in noise-induced cochlear injury and that increased inflammation can be considered a consequence of PPAR down-regulation induced by ROS production. Indeed, by decreasing oxidative stress, PPARs returned to control values, reactivating the negative control on inflammation in a feedback loop.
Lingua originaleEnglish
pagine (da-a)N/A-N/A
Numero di pagine19
Stato di pubblicazionePubblicato - 2021


  • Acoustic trauma
  • Anakinra
  • Cochlea
  • IL-1β
  • NF-κB
  • Q-ter
  • ROS


Entra nei temi di ricerca di 'Noise-induced cochlear damage involves ppar down-regulation through the interplay between oxidative stress and inflammation'. Insieme formano una fingerprint unica.

Cita questo