摘要
采用雄性豚鼠按每天50 mg/kg给予醋酸泼尼松龙肌注连续10 d,在第6天按每天400 mg/kg给予硫酸卡那霉素肌注连续5 d的方法,制备肾虚耳聋模型。将携带Mn SOD基因的慢病毒液经圆窗膜注入豚鼠耳蜗的外淋巴液中,并检测耳蜗外源性Mn SOD和Caspase 3的活性。以此研究锰超氧化物歧化酶(Mn SOD)基因对肾虚耳聋豚鼠耳蜗组织的Caspase 3蛋白活性的影响,探讨其对内耳氧化损伤的保护作用机制。结果表明外源性Mn SOD基因转染肾虚耳聋豚鼠耳蜗组织能够抑制其Caspase 3的蛋白活性,从而对内耳氧化损伤起到保护作用。
First, the model of kidney deficiency deafness was prepared, male guinea pigs were given 50 mg/kg/day prednisolone acetate for 10 days. Then from day 6 each guinea pigs were intramuscular injection kanamycin 400mg/kg/day. The lentiviral solution carrying manganese superoxide dismutase(Mn SOD) gene was injected into the perilymph of guinea pig cochlea through round window membrane, and the activities of exogenous Mn SOD and Caspase 3 were detected. In order to studied the effect of Mn SOD gene on the activity of Caspase 3 protein in cochlear tissue of guinea pigs with kidney vacuity deafness. And explored the protective mechanism of Mn SOD gene on oxidative damage in inner ear. The results showed that the cochlear tissue of guinea pigs transfected with exogenous Mn SOD gene could inhibit the activity of Caspase 3 protein and protect the inner ear from oxidative damage. Inhibit the activity of Caspase 3 protein, and thus protect the inner ear from oxidative damage.
出处
《浙江海洋学院学报(自然科学版)》
CAS
2017年第1期81-85,共5页
Journal of Zhejiang Ocean University(Natural Science Edition)
基金
浙江省教育厅科研项目(Y201121286)