PubMed · 2012 · 12 citations · 25 references
MedicineOtolaryngologyPharmacologyCell SignalingNeurotoxicologyOtologyAuditory NeurophysiologyAuditory PhysiologyCochlear FunctionCochlear NeurobiologyCochlear NeuroscienceOtotoxicityC-jun N-terminal Kinase SignalingCochlear ToxicityImmunohistochemical StainingJun N-terminal Kinase SignalingOtotoxicity MechanismsOtotoxicity PathophysiologyP38 Mitogen-activated Protein Kinase SignalingWestern Blot Analysis
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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Diabetes and Alpha Lipoic Acid
Saeid Golbidi, Mohammad Badran, Ismail Laher · Frontiers in Pharmacology · 2011 · 272 citations · Full text
Caspase-independent pathways of hair cell death induced by kanamycin in vivo
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