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Cited by (53)
Hearing Loss: Environmental, Sensorineural, Drug Induced (Cisplatinin, Antibiotics)
2022, Comprehensive PharmacologyKL1333, a derivative of β-lapachone, protects against cisplatin-induced ototoxicity in mouse cochlear cultures
2020, Biomedicine and PharmacotherapyCitation Excerpt :For example, adenosine A1 receptor (A1AR), a G protein-coupled receptor, plays a protective role by activating anti-inflammatory and antioxidative pathways in cochlear cells [11]. A1AR agonist was shown to increase activities of antioxidative enzymes, including glutathione peroxidase and superoxide dismutase, and to suppress the NOX3/STAT1-mediated inflammatory pathway [11,12]. Importantly, A1AR is distributed throughout the cochlea, including cells in the stria vascularis, spiral ganglion, and organ of Corti, with expression being greatest in IHCs and Deiters’ cells but much lower in OHCs [13].
Purinergic signaling in the organ of Corti: Potential therapeutic targets of sensorineural hearing losses
2019, Brain Research BulletinCitation Excerpt :Excitotoxicity caused by applying kainic acid into the perilymph was also attenuated by A1 agonists, but not effected by A2A agonists (Tabuchi et al., 2012). The idea that adenosine receptor activation recruits protective mechanism against the increased level of reactive oxygen species was supported by the elevation of superoxide dismutase, catalase or glutathione peroxidase activity detected in different models (Ford et al., 1997b, 1997a; Whitworth et al., 2004). The increase of cochlear blood flow by adenosine could contribute to its protective effect.
The effect of caffeine on hearing in a guinea pig model of acoustic trauma
2014, American Journal of Otolaryngology - Head and Neck Medicine and SurgeryThe effects of A1 and A2A adenosine receptor agonists on kainic acid excitotoxicity in the guinea pig cochlea
2012, Neuroscience LettersCitation Excerpt :Four subtypes of adenosine receptor, namely A1, A2A, A2b, and A3, have been cloned and characterized [10]. All subtypes have been identified in the cochlea [4,11]. Adenosine A1 receptor agonists reduce neuronal excitability and decrease firing rates by enhancing membrane hyperpolarization in the post-synaptic neurons [7,20].
Micellization of cisplatin (NC-6004) reduces its ototoxicity in guinea pigs
2012, Journal of Controlled ReleaseCitation Excerpt :To prevent CDDP ototoxicity without reducing its antitumor activity, these agents require invasive approaches for delivery into the inner ear. Several other agents that protect from CDDP ototoxicity and also preserve its antitumor effect have been developed; round window application of adenosine A1 receptor agonists [26,27] and oral administration of ebselen and allopurinol [28], sodium butyrate [29], and salicylates [30] are partially effective in reducing CDDP ototoxicity without affecting its antitumor activity in animals. Until now, however, no clinical interventions have been shown to prevent CDDP ototoxicity and ensure safe therapy without reduced antitumor activity [31].