AI Article Synopsis
- Glucocorticoids, like methylprednisolone, are effective in reducing cochlear injury caused by loud noises, but their exact protective mechanisms remain unclear.
- The study involved exposing mice to high decibel sounds and assessing their hearing through auditory brainstem responses while examining hair cell damage.
- Results showed that methylprednisolone and a phospholipase A2 inhibitor (quinacrine) helped reduce hearing loss and hair cell damage, while a glucocorticoid receptor inhibitor (RU486) negated the protective effects of methylprednisolone.
Article Abstract
Glucocorticoids are used clinically for the treatment of acoustic injury. However, the protective mechanism of glucocorticoid in acoustic injury has not been completely clarified. Also, the effects of phospholipase A2 (PLA2) on acoustic injury have not been examined to the best of our knowledge. The purpose of the present study was to examine the effects of methylprednisolone, a glucocorticoid receptor inhibitor (RU486) and a phospholipase A2 inhibitor (quinacrine) on cochlear injury induced by acoustic overexposure. Seventy-eight mice were exposed to a 4kHz pure tone at 128dB SPL for 4h. The auditory brainstem response (ABR) was used to examine the hearing thresholds. Cochlear morphology was examined to estimate the outer hair cell loss induced by acoustic overexposure. Methylprednisolone and quinacrine significantly alleviated the hearing threshold shift and hair cell loss induced by acoustic overexposure. RU486 antagonized the protective effect of methylprednisolone. The present findings suggest firstly that glucocorticoids exert protective effects against acoustic injury; secondly, that the protective effect of methylprednisolone was exerted by binding glucocorticoid receptors, and finally that activation of PLA2 may be involved in acoustic injury.
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| http://dx.doi.org/10.1016/j.neulet.2006.11.029 | DOI Listing |
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