Oxidative stress and inflammation cause auditory system damage via glial cell activation and dysregulated expression of gap junction proteins in an experimental model of styrene-induced oto/neurotoxicity.
Fabiola PacielloAnna PisaniRolando RolesiRaffaele MontuoroVeronica Mohamed-HizamGiammarco BoniCristian RipoliJacopo GalliRenata SistoAnna Rita FetoniClaudio GrassiPublished in: Journal of neuroinflammation (2024)
Collectively, our results provide novel evidence on the role of immune and glial cell activation in the oxidative/inflammatory damage induced by styrene in the auditory system at both peripheral and central levels, also involving alterations of gap junction networks. Our data suggest that targeting glial cells and connexin/pannexin expression might be useful to attenuate oxidative/inflammatory damage in the auditory system.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- poor prognosis
- dna damage
- working memory
- single cell
- ischemia reperfusion injury
- neuropathic pain
- cell therapy
- binding protein
- electronic health record
- mesenchymal stem cells
- long non coding rna
- stem cells
- endoplasmic reticulum stress
- drug induced
- cell death
- signaling pathway
- chemotherapy induced
- heat shock protein