Mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxicity

• Published in: Neural regeneration research 2012-12, Vol.7 (35), p.2793-2800
• Main Authors: Wang, Aimei, Hou, Ning, Bao, Dongyan, Liu, Shuangyue, Xu, Tao
• Format: Article
• Language: English
• Subjects: Acids; Antioxidants; Apoptosis; Autonomic Nerve Damage and Neural Regeneration; c-Jun; Experiments; Hair; Hearing loss; Kinases; Laboratory animals; Lipid peroxidation; Lipids; Noise; Oxidative stress; p38丝裂原活化蛋白激酶; Rodents; Signal transduction; Studies; α-硫辛酸; 免疫组化染色; 卡那霉素; 听性脑干反应; 毒性机制; 衰减
• ISSN: 1673-5374; 1876-7958
• 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. AIpha-lipoic acid effectively attenuated kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and phosphorylated c-Jun N-terminal kinase.