α-硫辛酸减轻卡那霉素耳毒性的机制。
Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity.
机构信息
Department of Physiology, Liaoning Medical University, Jinzhou 121001, Liaoning Province, China.
Scientific Laboratorial Center, Liaoning Medical University, Jinzhou 121001, Liaoning Province, China.
出版信息
Neural Regen Res. 2012 Dec 15;7(35):2793-800. doi: 10.3969/j.issn.1673-5374.2012.35.007.
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.
鉴于α-硫辛酸能有效预防顺铂和噪声等各种因素对耳蜗细胞的损伤的理论，本研究探讨了α-硫辛酸是否能预防卡那霉素诱导的耳毒性。为此，健康的 BALB/c 小鼠皮下注射α-硫辛酸和卡那霉素 14 天。听性脑干反应测试显示，卡那霉素引起的听觉脑干反应阈值移位显著受到抑制。免疫组化染色和 Western blot 分析显示，小鼠耳蜗中磷酸化 p38 丝裂原活化蛋白激酶和磷酸化 c-Jun N 端激酶的表达显著降低。实验结果表明，磷酸化 p38 和磷酸化 c-Jun N 端激酶介导了 BALB/c 小鼠中卡那霉素诱导的耳毒性损伤。α-硫辛酸通过抑制卡那霉素诱导的磷酸化 p38 和磷酸化 c-Jun N 端激酶的高表达，有效减轻了卡那霉素耳毒性。
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