About this item:

382 Views | 587 Downloads

Author Notes:

Correspondence and requests for materials should be addressed to Y.S. (email: sunyu@hust.edu.cn) or W.T. (email: wenxue.tang@yahoo.com).

Yu Sun & Jintao Yu contributed equally to this work.

W.X.T. and X.L. conceived and designed the study, and interpreted data.

W.X.T. and Y.S. carried out the experiments involving immunohistochemistry, western blot analysis, and generated the figures.

J.T.Y. and Y.S. analyzed data and drafted the paper.

All authors contributed to the data analysis and preparation of the manuscript.

The authors declare no competing financial interests.

Subjects:

Research Funding:

This research was supported in part by grants from the National Nature Science Foundation of China (81570923).

Keywords:

  • Otolaryngology
  • Experimental models of disease
  • Trauma

Inhibition of cyclooxygenase-2 by NS398 attenuates noise-induced hearing loss in mice

Tools:

Journal Title:

Scientific Reports

Volume:

Volume 6

Publisher:

, Pages 22573-22573

Type of Work:

Article | Final Publisher PDF

Abstract:

Noise-induced hearing loss (NIHL) is an important occupational disorder. However, the molecular mechanisms underlying NIHL have not been fully clarified; therefore, the condition lacks effective therapeutic methods. Cyclooxygenase-2 (Cox-2) is an inducible enzyme involved in the synthesis of prostaglandins, and has been implicated in many pathophysiological events, such as oxidative stress and inflammation. In this study, we investigated the possible role of Cox-2 in the mechanisms of NIHL and the therapeutic effect of the Cox-2 inhibitor NS398 on NIHL using a mouse model. We demonstrated that Cox-2 is constitutively expressed in the mouse cochlea, and its expression could be dramatically up-regulated by high levels of noise exposure. Furthermore, we demonstrated that pre-treatment with the Cox-2 inhibitor NS398 could inhibit Cox-2 expression during noise overstimulation; and could attenuate noise-induced hearing loss and hair cell damage. Our results suggest that Cox-2 is involved in the pathogenesis of NIHL; and pharmacological inhibition of Cox-2 has considerable therapeutic potential in NIHL.

Copyright information:

© 2016, Macmillan Publishers Limited

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/).

Creative Commons License

Export to EndNote