The effects of the glucocorticoid receptor antagonist RU486 and phospholipase A2 inhibitor quinacrine on acoustic injury of the mouse cochlea

The effects of the glucocorticoid receptor antagonist RU486 and phospholipase A2 inhibitor quinacrine on acoustic injury of the mouse cochlea
复制标题

DOI:
10.1016/j.neulet.2006.11.029
复制
发表时间:
2007-02-08
影响因子:
2.5
通讯作者:
Hara, Akira
Hara, Akira
中科院分区:
医学4区
文献类型:
--
作者:
Hirose, Yuki;Tabuchi, Keiji;Hara, Akira

文献摘要

被引文献

相似文献

糖皮质激素在临床上用于治疗声损伤。但糖皮质激素在声损伤中的保护机制尚未完全阐明。此外,磷脂酶A2(PLA 2)对声损伤的影响还没有被检查到最好的我们的知识。本研究的目的是探讨甲基强的松龙,糖皮质激素受体抑制剂(RU 486)和磷酸脂酶A2抑制剂(奎纳克林)对耳蜗损伤的影响。78只小鼠暴露于128 dB SPL的4 kHz纯音中4 h。采用听性脑干反应(ABR)检测听阈。检查耳蜗形态学以估计由声过度照射引起的外毛细胞损失。甲基强的松龙和奎纳克林可明显减轻声刺激引起的听阈偏移和毛细胞丢失。RU 486拮抗甲基强的松龙的保护作用。目前的研究结果表明,首先,糖皮质激素发挥保护作用,对声损伤;其次,甲基强的松龙的保护作用是通过结合糖皮质激素受体,最后,PLA 2的激活可能参与了声损伤。(c)2006爱思唯尔爱尔兰有限公司保留所有权利。
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 phosphlipase A2 inhibitor (quinacrine) on cochlear injury induced by acoustic overexposure. Seventy-eight mice were exposed to a 4 kHz pure tone at 128 dB SPL for 4 h. 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. (c) 2006 Elsevier Ireland Ltd. All rights reserved.