Abstract
BackgroundA reduction in cochlear blood flow plays an essential role in noise-induced hearing loss (NIHL). The timely regulation of cochlear perfusion determines the progression and prognosis of NIHL. Hydrogen sulfide (H2S) has attracted increasing interest as a vasodilator in cardiovascular systems. This study identified the role of H2S in cochlear blood flow regulation and noise protection.Methodology/Principal FindingsThe gene and protein expression of the H2S synthetase cystathionine-γ-lyase (CSE) in the rat cochlea was examined using immunofluorescence and real-time PCR. Cochlear CSE mRNA levels varied according to the duration of noise exposure. A chronic intracochlear infusion model was built and artificial perilymph (AP), NaHS or DL-propargylglycine (PPG) were locally administered. Local sodium hydrosulfide (NaHS) significantly increased cochlear perfusion post-noise exposure. Cochlear morphological damage and hearing loss were alleviated in the NaHS group as measured by conventional auditory brainstem response (ABR), cochlear scanning electron microscope (SEM) and outer hair cell (OHC) count. The highest percentage of OHC loss occurred in the PPG group.Conclusions/SignificanceOur results suggest that H2S plays an important role in the regulation of cochlear blood flow and the protection against noise. Further studies may identify a new preventive and therapeutic perspective on NIHL and other blood supply-related inner ear diseases.
Highlights
Noise-induced hearing loss (NIHL) is a sensorineural hearing loss that results from noise-induced cochlear hair cell damage
Endothelin, a-adrenergic receptors, peptide-containing nerve fibers, and sphingosine-1-phosphate receptors participate in the constriction of spiral modiolar artery (SMA) [6,7,8,9,10,11,12], and nitric oxide (NO) and calcitonin gene-related protein (CGRP) regulate the relaxation of SMA [13,14]
To show that H2S may play a role in noise-induced hearing loss (NIHL), cochlear CSE mRNA expression and auditory brainstem response (ABR) threshold shifts were analyzed after different durations of noise exposure
Summary
Noise-induced hearing loss (NIHL) is a sensorineural hearing loss that results from noise-induced cochlear hair cell damage. To show that H2S may play a role in NIHL, cochlear CSE mRNA expression and auditory brainstem response (ABR) threshold shifts were analyzed after different durations of noise exposure. Statistical analyses revealed that the percent of OHC loss in the first row increased in the PPG group and decreased significantly in the NaHS group (ANOVA, F = 11.83, p,0.01; SNK test, p,0.05). The disarrangement of OHC stereociliary bundles was least obvious in the NaHS group compared to the other groups These results suggested that exogenous H2S administration protected the cochlea against noise damage. The ABR threshold shift demonstrated a significant decrease in the NaHS group (47.0062.60 dB SPL) compared to the other groups (SNK, P,0.05) These results suggested a functionally protective effect of H2S against NIHL
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