Electronic Resource
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
العنوان: | 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 |
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المؤلفون: | Paciello, Fabiola, Pisani, Anna, Rolesi, Rolando, Montuoro, Raffaele, Mohamed Hizam, Veronica, Boni, Giammarco, Ripoli, Cristian, Galli, Jacopo, Sisto, Renata, Fetoni, Anna Rita, Grassi, Claudio, Paciello, Fabiola (ORCID:0000-0002-8473-8074), Mohamed-Hizam, Veronica, Ripoli, Cristian (ORCID:0000-0002-5315-0163), Galli, Jacopo (ORCID:0000-0001-6353-6249), Fetoni, Anna Rita (ORCID:0000-0001-5405-4301), Grassi, Claudio (ORCID:0000-0001-7253-1685) |
بيانات النشر: | BMC 2024 |
نوع الوثيقة: | Electronic Resource |
مستخلص: | BackgroundRedox imbalance and inflammation have been proposed as the principal mechanisms of damage in the auditory system, resulting in functional alterations and hearing loss. Microglia and astrocytes play a crucial role in mediating oxidative/inflammatory injury in the central nervous system; however, the role of glial cells in the auditory damage is still elusive.ObjectivesHere we investigated glial-mediated responses to toxic injury in peripheral and central structures of the auditory pathway, i.e., the cochlea and the auditory cortex (ACx), in rats exposed to styrene, a volatile compound with well-known oto/neurotoxic properties.MethodsMale adult Wistar rats were treated with styrene (400 mg/kg daily for 3 weeks, 5/days a week). Electrophysiological, morphological, immunofluorescence and molecular analyses were performed in both the cochlea and the ACx to evaluate the mechanisms underlying styrene-induced oto/neurotoxicity in the auditory system.ResultsWe showed that the oto/neurotoxic insult induced by styrene increases oxidative stress in both cochlea and ACx. This was associated with macrophages and glial cell activation, increased expression of inflammatory markers (i.e., pro-inflammatory cytokines and chemokine receptors) and alterations in connexin (Cxs) and pannexin (Panx) expression, likely responsible for dysregulation of the microglia/astrocyte network. Specifically, we found downregulation of Cx26 and Cx30 in the cochlea, and high level of Cx43 and Panx1 in the ACx.ConclusionsCollectively, 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. |
مصطلحات الفهرس: | Astrogliosis, Auditory cortex, Cochlea, Gap junctions, Macrophages, Microglia morphology, Pro-inflammatory cytokines, ROS, Settore BIO/09 - FISIOLOGIA, info:eu-repo/semantics/article |
URL: | info:eu-repo/semantics/altIdentifier/pmid/38178142 info:eu-repo/semantics/altIdentifier/wos/WOS:001136874500010 volume:21 issue:1 firstpage:N/A lastpage:N/A numberofpages:18 issueyear:2024 journal:JOURNAL OF NEUROINFLAMMATION |
الاتاحة: | Open access content. Open access content info:eu-repo/semantics/openAccess |
ملاحظة: | English |
Other Numbers: | SYC oai:publicatt.unicatt.it:10807/261336 10.1186/s12974-023-02996-3 info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85181235354 1439664650 |
المصدر المساهم: | UNIV CATTOLICA DEL SACRO CUORE From OAIster®, provided by the OCLC Cooperative. |
رقم الانضمام: | edsoai.on1439664650 |
قاعدة البيانات: | OAIster |
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