1.The possible mechanism of alpha-lipoic acid in attenuating kanamycin-induced ototoxic injury was verified in accordance with the antioxidant properties of alpha-lipoic acid.
2.Phosphorylated p38 mitogen-activated protein kinase and c-Jun N-terminal kinase mediate kanamycin-induced ototoxic injury in BALB/c mice. Alpha-lipoic acid can effectively attenuate kanamycin ototoxicity by inhibiting the kanamycin-induced high expression of phosphorylated p38 and c-Jun N-terminal kinase.
3.The pathway of alpha-lipoic acid for neuronal ototoxicity protection was investigated to provide a theoretical basis for the treatment of drug-induced deafness in clinic.
1.实验依据α-硫辛酸具有抗氧化剂的特点,旨在验证其可能具有防护卡那霉素而损伤效应的机制。
2.结果显示,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BALB/c小鼠的耳毒性损伤。α-硫辛酸可显著抑制卡那霉素所致磷酸化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的耳毒性。实验揭示了α-硫辛酸对神经耳毒性防护的作用途径,为临床药物性耳聋的防治提供了理论依据。