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新生大鼠的溶血会导致听觉损伤。

Hemolysis in neonatal rats results in auditory impairment.

作者信息

Li Qi, Chen Peipei, Guo Weiwei, Fang Ruping, Yang Shiming

机构信息

Department of Otolaryngology, Nanjing Children's Hospital, Nanjing Medical University , Nanjing , Jiangsu.

出版信息

Acta Otolaryngol. 2014 Nov;134(11):1114-20. doi: 10.3109/00016489.2014.938361.

DOI:10.3109/00016489.2014.938361
PMID:25315910
Abstract

CONCLUSION

This study suggests that hyperbilirubinemia in the neonatal rat can impair auditory function and induce peripheral nerve pathology by reducing neurofilament-positive cells in spiral ganglion neurons (SGNs). This finding indicates a potential connection between hyperbilirubinemia and auditory impairment.

OBJECTIVE

To establish a neonatal rat hyperbilirubinemia induced by hemolysis and assess the possible link between hyperbilirubinemia and auditory impairment.

METHODS

Wistar rats were divided into two groups - a bilirubin exposure group injected with phenylhydrazine hydrochloride at 7 and 28 days of age to induce hyperbilirubinemia, and a control group given saline. Auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAEs) were determined to assess auditory function. Cochlea basilar membrane stretch preparations and cochlear frozen sections were examined for morphological changes in hair cells and SGNs.

RESULTS

At day 7, ABR wave I, III, and V latencies, and I-III, I-V interwave intervals (IWIs) in the experimental group were significantly prolonged compared with those in the control group. ABR thresholds were also elevated in the experimental group. We found no significant difference in DPOAEs in the bilirubin exposure group compared to the control group. The ABRs and DPOAEs in the experimental group were restored at age 28 days. Cochlear hair cells showed no signs of loss in either group; however, the total number of neurofilament-positive cells in SGNs was significantly reduced in the phenylhydrazine-treated animals.

摘要

结论

本研究表明,新生大鼠高胆红素血症可通过减少螺旋神经节神经元(SGNs)中神经丝阳性细胞来损害听觉功能并诱发周围神经病变。这一发现表明高胆红素血症与听觉障碍之间存在潜在联系。

目的

建立溶血诱导的新生大鼠高胆红素血症模型,并评估高胆红素血症与听觉障碍之间的可能联系。

方法

将Wistar大鼠分为两组——胆红素暴露组,在7日龄和28日龄时注射盐酸苯肼以诱导高胆红素血症;对照组给予生理盐水。测定听觉脑干反应(ABR)和畸变产物耳声发射(DPOAE)以评估听觉功能。检查耳蜗基底膜拉伸标本和耳蜗冰冻切片,观察毛细胞和SGNs的形态变化。

结果

在7日龄时,与对照组相比,实验组的ABR波I、III和V潜伏期以及I-III、I-V波间期(IWIs)显著延长。实验组的ABR阈值也升高。与对照组相比,胆红素暴露组的DPOAE没有显著差异。实验组在28日龄时ABR和DPOAE恢复正常。两组耳蜗毛细胞均无丢失迹象;然而,在苯肼处理的动物中,SGNs中神经丝阳性细胞的总数显著减少。

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