Protection of cochlear function from aminoglycosides ototoxicity by manganese superoxide dismutase gene in aging rat.
- Author:
Yang YANG
1
;
Wei-jia KONG
;
Yu-juan HU
;
Jun LI
;
Yi ZHONG
;
Xue-yan ZHAO
;
Ya-nan HAO
;
Wei PENG
Author Information
- Publication Type:Journal Article
- MeSH: Aminoglycosides; adverse effects; Animals; Apoptosis; drug effects; Caspase 3; metabolism; Cochlea; metabolism; pathology; Dependovirus; genetics; Ear, Inner; cytology; metabolism; Female; Genetic Therapy; Genetic Vectors; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; genetics; Transfection
- From: Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2009;44(8):657-663
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEdetermine the feasibility of manganese superoxide dismutase (MnSOD) gene therapy for protecting the cochlear function against aminoglycoside-induced oxidative stress in aging rats.
METHODSThe 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.
RESULTSCompared 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).
CONCLUSIONSMnSOD could play a partly role to treat cochlear aminoglycoside-induced oxidative damage in aging rats.
