C-Phycocyanin Attenuates Noise-Induced Cochlear Synaptopathy via the Inhibition of Oxidative Stress and Intercellular Adhesion Molecule-1 in the Cochlea

• Published in: International journal of molecular sciences 2024-05, Vol.25 (10), p.5154
• Main Authors: Lin, Yi-Chun, Shih, Cheng-Ping, Lin, Yuan-Yung, Lin, Hung-Che, Kuo, Chao-Yin, Chen, Hang-Kang, Chen, Hsin-Chien, Wang, Chih-Hung
• Format: Article
• Language: English
• Subjects: Analysis; Animals; Antioxidants; Antioxidants - pharmacology; C-phycocyanin; Cell Line; Cochlea - drug effects; Cochlea - metabolism; Cochlea - pathology; cochlear synaptopathy; Cytotoxicity; Enzymes; Guinea Pigs; Hair Cells, Auditory, Inner - drug effects; Hair Cells, Auditory, Inner - metabolism; Hair Cells, Auditory, Inner - pathology; Hearing loss; Hearing Loss, Hidden; Hearing Loss, Noise-Induced - drug therapy; Hearing Loss, Noise-Induced - metabolism; Hearing Loss, Noise-Induced - pathology; Hearing protection; Hydrogen Peroxide - metabolism; inner hair cell; Intercellular Adhesion Molecule-1 - metabolism; Ligaments; Lipid peroxidation; Male; noise; Noise - adverse effects; Noise control; Oxidative stress; Oxidative Stress - drug effects; Pathogenesis; Phycocyanin - pharmacology; Phycocyanin - therapeutic use; Proteins; Reactive oxygen species; Reactive Oxygen Species - metabolism; Scientific equipment and supplies industry; Spiral Ganglion - drug effects; Spiral Ganglion - metabolism; Spiral Ganglion - pathology; Synapses; Synapses - drug effects; Synapses - metabolism; Toxicity; Yang Mu
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms25105154

The synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) are the most vulnerable structures in the noise-exposed cochlea. Cochlear synaptopathy results from the disruption of these synapses following noise exposure and is considered the main cause of poor speech understanding in noisy environments, even when audiogram results are normal. Cochlear synaptopathy leads to the degeneration of SGNs if damaged IHC-SGN synapses are not promptly recovered. Oxidative stress plays a central role in the pathogenesis of cochlear synaptopathy. C-Phycocyanin (C-PC) has antioxidant and anti-inflammatory activities and is widely utilized in the food and drug industry. However, the effect of the C-PC on noise-induced cochlear damage is unknown. We first investigated the therapeutic effect of C-PC on noise-induced cochlear synaptopathy. In vitro experiments revealed that C-PC reduced the H O -induced generation of reactive oxygen species in HEI-OC1 auditory cells. H O -induced cytotoxicity in HEI-OC1 cells was reduced with C-PC treatment. After white noise exposure for 3 h at a sound pressure of 118 dB, the guinea pigs intratympanically administered 5 μg/mL C-PC exhibited greater wave I amplitudes in the auditory brainstem response, more IHC synaptic ribbons and more IHC-SGN synapses according to microscopic analysis than the saline-treated guinea pigs. Furthermore, the group treated with C-PC had less intense 4-hydroxynonenal and intercellular adhesion molecule-1 staining in the cochlea compared with the saline group. Our results suggest that C-PC improves cochlear synaptopathy by inhibiting noise-induced oxidative stress and the inflammatory response in the cochlea.