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Updated: Jun 18, 2026
The Mouse Round-window Approach for Ototoxic Agent Delivery: A Rapid and Reliable Technique for Inducing Cochlear Cell Degeneration
Published on: November 26, 2015
[Protection of cochlear function from aminoglycosides ototoxicity by manganese superoxide dismutase gene in aging
Yang Yang1, Wei-jia Kong, Yu-juan Hu
1Department of Otorhinolaryngology Head and Neck Surgery, Union Hospital of Tongji medical college, Huazhong University of Science and Technology, Wuhan 430022, China.
Objective:
determine the feasibility of manganese superoxide dismutase (MnSOD) gene therapy for protecting the cochlear function against aminoglycoside-induced oxidative stress in aging rats.
Methods:
The aging model of SD rats were obtained with 8 weeks daily of D-gal (150 mg/kg per day) hypodermic injection. In the 9th week, amikacin (500 mg/kg per day) were injected intramuscularly into some aging SD rats. The viral particles of recombinant adeno-associated viral vector II/MnSOD (6 microl, 5 x 10(11) vector genomes/ml) were injected into the perilymph through the round window membrane (RWM). The feasibility of MnSOD gene therapy against aminoglycoside-induced oxidative stress in aging rats was evaluated with the methods of caspase-3 protein analysis, apoptosis detection with immunohistochemical, the detection of MnSOD concentration, stretched preparation of basilar membrane and evaluation of hearing threshold with ABR-click.
Results:
Compared with the control group, the concentration of MnSOD of cochlear tissue was increased (P < 0.05), and the active fragment expression of caspase-3, the numbers of apoptosis bodies and the hearing threshold were decreased (P < 0.05).
Conclusions:
MnSOD could play a partly role to treat cochlear aminoglycoside-induced oxidative damage in aging rats.
