【每日动态】氢气治疗听神经损伤

来自第四军医大学西京医院关于呼吸氢气治疗硅巴因诱导的听神经病，发表在《中国药理学报》。

听神经病是一种听觉障碍，其特征是听毛细胞正常但神经功能异常。氢气作为一种抗氧化抗炎症抗细胞凋亡物质在许多疾病模型和临床研究中证明具有治疗作用，本研究主要是为探索氢气是否对硅巴因诱导的听神经病具有治疗作用。氢气在呼吸气体中的浓度分别为1%, 2%, and 4%，分别在硅巴因后1小时和6小时呼吸60分钟氢气混合气。在硅巴因诱导前和7天后，用听觉脑干诱发电位检测动物听力状态，用畸变产物耳声发射(DPOAE) 测定听细胞功能。7天后用形态学分析耳蜗和神经节。Tunel染色和caspase3免疫组织化学染色评价神经节细胞凋亡情况。结果发现，硅巴因可以诱导脑干听力诱发电位的低单音和短纯音（click and tone）在4、8、16Hz听阈移位，呼吸2%和4%的氢气能显著改善该作用。硅巴因和氢气对DPOAE均无影响。形态学结果表明2%氢气可减轻硅巴因诱导的神经节损伤和细胞凋亡。但对听毛细胞没有影响。结果表明，氢气氢气可以改善硅巴因诱导的听神经病。

本研究证明氢气可以保护听神经，结合过去日本和中国学者对氢气保护噪声性耳聋治疗的研究，氢气不仅可以保护听毛细胞，而且可以保护听神经损伤。那么氢气作为耳聋，特别是急性期患者的治疗价值将值得期待。

Acta PharmacolSin. 2012 Mar 5. doi: 10.1038/aps.2011.190. [Epub ahead of print]

Inhalation of hydrogengas attenuates ouabain-induced

auditoryneuropathy in gerbils.

Qu J, Gan YN, Xie KL, Liu WB, Wang YF, Hei RY, Mi WJ, Qiu JH.

Source

Department of Otolaryngology, Xijing Hospital, Fourth Military MedicalUniversity, Xi'an 710032, China.

Abstract

Aim:Auditory neuropathy (AN) is a hearing disorder characterized byabnormal auditory nerve function with preservation of normal cochlear haircells. This study was designed to investigate whether treatment with molecular hydrogen(H(2)), which can remedy damage in various organs via reducing oxidativestress, inflammation and apoptosis, is beneficial to ouabain-induced AN ingerbils.Methods:AN model was made by local application of ouabain (1 mmol/L, 20mL) to the round window membrane in male Mongolian gerbils. H(2) treatment wasgiven twice by exposing the animals to H(2) (1%, 2%, and 4%) for 60 min at 1 hand 6 h after ouabain application. Before and 7 d after ouabain application,the hearing status of the animals was evaluated using the auditory brainstemresponse (ABR) approach, the hear cell function was evaluated with distortionproduct otoacoustic emissions (DPOAE). Seven days after ouabain application,the changes in the cochleae, especially the spiral ganglion neurons (SGNs),were morphologically studied. TUNEL staining and immunofluorescent staining foractivated caspase-3 were used to assess the apoptosis of SGNs.Results:Treatmentwith H(2) (2% and 4%) markedly attenuated the click and tone burst-evoked ABRthreshold shift at 4, 8, and 16 kHz in ouabain-exposed animals. Neither localouabain application, nor H(2) treatment changed the amplitude of DPOAE at 4, 8,and 16 kHz. Morphological study showed that treatment with H(2) (2%)significantly alleviated SGN damage and attenuated the loss of SGN density foreach turn of cochlea in ouabain-exposed animals. Furthermore, ouabain causedsignificantly higher numbers of apoptotic SGNs in the cochlea, which wassignificantly attenuated by the H(2) treatment. However, ouabain did not changethe morphology of cochlear hair cells.Conclusion:The results demonstrate thatH(2) treatment is beneficial to ouabain-induced AN via reducing apoptosis.Thus, H(2) might be a potential agent for treating hearing impairment in AN