Prevention of trauma-induced cochlear fibrosis using intracochlear application of anti-inflammatory and antiproliferative drugs

Highlights • Inflammation and epithelial to mesenchymal cell transition are involved in cochlear fibrosis. • Dexamethasone and aracytine both prevent fibrosis in the cochlea. • Analysis of the risk/benefit ratio favors the use of Ara-C to prevent cochlear fibrosis.

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Bibliographische Detailangaben
Veröffentlicht in:	Neuroscience 2016-03, Vol.316, p.261-278
Hauptverfasser:	Jia, H, François, F, Bourien, J, Eybalin, M, Lloyd, R.V, Van De Water, T.R, Puel, J.-L, Venail, F
Format:	Artikel
Sprache:	eng
Schlagworte:	Adjuvants, Immunologic - toxicity Animals Anti-Inflammatory Agents - pharmacology aracytine Cochlea - drug effects Cochlea - injuries Cochlea - pathology Cochlea - ultrastructure cochlear implant Collagen - metabolism Cytokines - metabolism dexamethasone Dexamethasone - pharmacology Disease Models, Animal Electrodes, Implanted - adverse effects Evoked Potentials, Auditory, Brain Stem - drug effects Fibronectins - metabolism fibrosis Fibrosis - drug therapy Fibrosis - etiology Hair Cells, Auditory - drug effects Hair Cells, Auditory - pathology Hemocyanins - toxicity In Vitro Techniques Laminin - metabolism Neurology Organ Culture Techniques Rats Rats, Wistar Sensory Receptor Cells - drug effects Time Factors Tympanis Wounds and Injuries - complications
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Beschreibung
Zusammenfassung:	Highlights • Inflammation and epithelial to mesenchymal cell transition are involved in cochlear fibrosis. • Dexamethasone and aracytine both prevent fibrosis in the cochlea. • Analysis of the risk/benefit ratio favors the use of Ara-C to prevent cochlear fibrosis.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2015.12.031