The histone deacetylase inhibitor sodium butyrate protects against noise-induced hearing loss in Guinea pigs. (1st November 2017)

• Record Type: Journal Article
• Authors: Yang, Deng-Hua; Xie, Jing; Liu, Ke; Peng, Zhe; Guo, Jing-Ying; Yu, Shu-Kui; Wang, Guo-Peng; Gong, Shu-Sheng
• Is Part Of: Neuroscience letters. Volume 660(2017)
• Page Start: 140
• Page End: 146
• Publication Date: 2017-11-01
• Subjects: 3-NT 3-nitrotyrosine -- DAPI 4′, 6-diamidino-2-phenylindole -- ABR auditory brainstem response -- HATs histone acetyltransferases -- HDACs histone deacetylases -- H3-AcK9 acetyl-histone H3 (Lys9) -- HC hair cell -- IHC inner hair cell -- NIHL noise-induced hearing loss -- OHC outer hair cell -- PBS phosphate buffered saline -- PC pillar cell -- PTS permanent threshold shift -- SAHA suberoylanilide hydroxamic acid -- SB sodium butyrate -- SPL sound pressure level -- TTS temporary threshold shift; Noise-induced hearing loss -- Sodium butyrate -- Histone -- Histone deacetylase inhibitor -- Oxidative stress -- Epigenetics; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.09.036
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Sodium butyrate (SB) inhibits histone deacetylation and oxidative stress after noise. SB attenuates noise-induced permanent threshold shifts and outer hair cell loss. SB may represent a potential strategy to prevent noise induced hearing loss. Abstract: Noise-induced hearing loss (NIHL) severely impacts the quality of life of affected individuals. Oxidative stress resulting from noise exposure is a significant cause of NIHL. Although histone deacetylase (HDAC) inhibitors were shown to protect against NIHL, the underlying mechanism remains unclear, and it is not known how they act on noise-induced oxidative stress. In the current study, we investigated the expression levels of acetyl-histone H3 (Lys9) (H3-AcK9), histone deacetylase 1 (HDAC1), and 3-nitrotyrosine (3-NT), an oxidative stress marker, in a guinea pig model of NIHL using immunohistology and Western blotting. We then assessed the effects of systemic administration of the HDAC inhibitor, sodium butyrate (SB), on noise-induced permanent threshold shifts (PTS), hair cell (HC) loss, and changes in the above mentioned markers. The results showed that SB attenuated noise-induced PTS and outer hair cell loss. SB treatment promoted H3-AcK9 expression and repressed HDAC1 expression in the nuclei of HCs and Hensen's cells after noise exposure. Furthermore, SB attenuated the noise-induced increase of 3-NT expression in HCs and Hensen's cells. These findings suggest that SB protects against NIHL by reversing the noise-induced histone acetylation imbalance and inhibiting oxidative stress in cochlear HCs and Hensen's cells. SB treatment may represent a potential strategy to prevent and treat NIHL.