Neural Regen Res：α-硫辛酸减轻卡那霉素致耳蜗损伤

α-硫辛酸能高效清除多种氧自由基，预防体内氧化应激的发生，近年来的研究证明其还具有防护顺铂、噪声等对大鼠、豚鼠耳蜗细胞损伤的作用。《中国神经再生研究（英文版）》杂志于2012年12月35期出版的一项关于“Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity”的研究显示，注射α-硫辛酸的卡那霉素耳毒性模型小鼠听脑干反应阈移明显受到抑制，耳蜗磷酸化p38丝裂原活化蛋白激酶和c-Jun氨基末端激酶表达亦明显减弱。提示磷酸化p38丝裂原活化蛋白激酶和c-Jun氨基末端激酶介导了卡那霉素对小鼠的耳毒性损伤，α-硫辛酸可显着抑制卡那霉素诱导的小鼠耳蜗中磷酸化p38丝裂原活化蛋白激酶和c-Jun氨基末端激酶的高表达，从而有效减轻卡那霉素对小鼠的耳毒性损伤。该研究对临床药物性耳聋的防治提供了理论依据。

doi:10.3969/j.issn.1673-5374.2012.35.007
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Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity

Aimei Wang1, Ning Hou1, Dongyan Bao1, Shuangyue Liu1, Tao Xu2

In view of the theory that alpha-lipoic acid effectively prevents cochlear cells from injury caused by various factors such as cisplatin and noise, this study examined whether alpha-lipoic acid can prevent kanamycin-induced ototoxicity. To this end, healthy BALB/c mice were injected subcutaneously with alpha-lipoic acid and kanamycin for 14 days. Auditory brainstem response test showed that increased auditory brainstem response threshold shifts caused by kanamycin were significantly inhibited. Immunohistochemical staining and western blot analysis showed that the expression of phosphorylated p38 mitogen-activated protein kinase and phosphorylated c-Jun N-terminal kinase in mouse cochlea was significantly decreased. The experimental findings suggest that phosphorylated p38 and phosphorylated c-Jun N-terminal kinase mediated kanamycin-induced ototoxic injury in BALB/c mice. Alpha-lipoic acid effectively attenuated kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and phosphorylated c-Jun N-terminal kinase.

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