Ye Hai-Bo, Wang Jian, Zhang Wei-Tian, Shi Hai-Bo, Yin Shan-Kai
Department of Otorhinolaryngology, Affiliated Sixth People's Hospital of Shanghai Jiaotong University, 600 Yishan Road, Shanghai 200233, China.
Int J Pediatr Otorhinolaryngol. 2013 May;77(5):647-54. doi: 10.1016/j.ijporl.2012.11.037. Epub 2012 Dec 27.
Previous work showed that taurine protects neurons against unconjugated bilirubin (UCB)-induced neurotoxicity by maintaining intracellular calcium homeostasis, membrane integrity, and mitochondrial function, thereby preventing apoptosis from occurring, in primary neuron cultures. In this study, we investigated whether taurine could protect the auditory system against the neurotoxicity associated with hyperbilirubinemia in an in vivo model.
Hyperbilirubinemia was established in neonatal guinea pigs by intraperitoneal injection of UCB. Hearing function was observed in electrocochleograms (ECochGs) and auditory brainstem responses (ABRs) recorded before and 1, 8, 24, and 72 h after UCB injection. For morphological evaluations, animals were sacrificed at 8h post-injection, and the afferent terminals beneath the inner hair cells (IHCs), spiral ganglion neurons (SGNs), and their fibers were examined.
It was found that UCB injection significantly increased latencies and inter-wave intervals, and thresholds of ABR and compound action potentials, and caused marked damage to type I SGNs, their axons, and terminals to cochlear IHCs. When baby guinea pigs were pretreated with taurine for 5 consecutive days and then injected with bilirubin, electrophysiological abnormalities and morphological damage were attenuated significantly in both the peripheral and central auditory system.
From these observations, it was concluded that taurine limited bilirubin-induced neural damage in the auditory system. These findings may contribute to the development of taurine as a broad-spectrum agent for preventing and/or treating hearing loss in neonatal jaundice.
先前的研究表明，在原代神经元培养中，牛磺酸通过维持细胞内钙稳态、膜完整性和线粒体功能来保护神经元免受未结合胆红素（UCB）诱导的神经毒性，从而防止细胞凋亡的发生。在本研究中，我们调查了在体内模型中牛磺酸是否可以保护听觉系统免受与高胆红素血症相关的神经毒性。
通过腹腔注射UCB在新生豚鼠中建立高胆红素血症。在注射UCB前以及注射后1、8、24和72小时记录电耳蜗图（ECochGs）和听觉脑干反应（ABRs），观察听力功能。为了进行形态学评估，在注射后8小时处死动物，并检查内毛细胞（IHCs）下方的传入终末、螺旋神经节神经元（SGNs）及其纤维。
发现注射UCB显著增加了ABR和复合动作电位的潜伏期、波间期和阈值，并对I型SGNs、其轴突以及耳蜗IHCs的终末造成了明显损伤。当幼豚鼠连续5天用牛磺酸预处理然后注射胆红素时，外周和中枢听觉系统的电生理异常和形态学损伤均显著减轻。
从这些观察结果得出结论，牛磺酸可限制胆红素诱导的听觉系统神经损伤。这些发现可能有助于将牛磺酸开发为预防和/或治疗新生儿黄疸听力损失的广谱药物。
