Styrene targets sensory and neural cochlear function through the crossroad between oxidative stress and inflammation

Fetoni, Anna Rita; Paciello, Fabiola; Rolesi, Rolando; Pisani, Anna; Moleti, Arturo; Sisto, Renata; Troiani, Diana; Paludetti, Gaetano; Grassi, Claudio

doi:10.1016/j.freeradbiomed.2020.12.001

Cited by 14 publications

(19 citation statements)

References 65 publications

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“…Indeed, noise exposure has been shown to up-regulate cochlear production of cytokines [ 5 , 6 , 7 ], such as interleukin 1-β (IL-1β), that have been observed after ROS generation in the cochlea [ 8 ]. Similar mechanisms have been reported to occur in drug-induced hearing loss [ 9 , 10 ] and aging [ 11 ].…”

Section: Introductionsupporting

confidence: 77%

“…At day 21 from noise exposure, after ABR recordings, animals were sacrificed with a lethal dose of anesthetic and the right cochleae of 6 animals/group were processed to perform IHC and OHC count. As described previously [ 10 , 14 ], to perform F-Actin staining, samples were fixed in 4% paraformaldehyde and incubated with Actin Green 488 Ready Probes Reagent (ThermoFisher, Waltham, MA, USA, Cat. No.…”

Section: Methodsmentioning

confidence: 99%

“…To determine the noise effect on spiral ganglion neurons (SGNs) survival, 6 cochleae/group (from 6 animals) were processed at 21 days after noise exposure. As described previously [ 10 ], cochleae were quickly removed and the samples were fixed with 4% paraformaldehyde in PBS at 4 °C and at pH 7.5. Next, the cochleae were decalcified for 15 days in EDTA (10%), incubated for 48 h in sucrose (30%), embedded in OCT and longitudinal sections (12 μM thickness) were obtained by using a cryostat (Cryostat CM 1950; SLEE).…”

Section: Methodsmentioning

confidence: 99%

“…Immunofluorescence analysis were performed on cochlear cryosections 1, 3 and 7 days after the acoustic trauma. As described previously [ 10 , 16 ], 12 cochleae of 6 animals/group were quickly removed and samples were fixed with 4% paraformaldehyde in PBS at 4 °C and pH 7.4. Next, the cochleae were decalcified for 15 days in EDTA (10% EDTA, changed daily), incubated for 48 h in sucrose (30%), embedded in OCT, cryosectioned at a thickness of 12 μM (Cryostat SLEE) and processed for each immunostaining procedure.…”

Section: Methodsmentioning

confidence: 99%

“…We have previously reported that in animal models of exogenous insults as noise exposure or ototoxic drugs, it is possible to attenuate hearing loss and cochlear damage by targeting the endogenous antioxidant system, [ 10 , 12 , 13 , 14 ]. Indeed, we obtained significant ROS reduction and hearing loss amelioration by using antioxidants such as polyphenols and CoQ10 analogues [ 12 , 15 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

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Noise-Induced Cochlear Damage Involves PPAR Down-Regulation through the Interplay between Oxidative Stress and Inflammation

et al. 2021

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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.

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