咬合干扰致大鼠咬肌氧化应激损伤及其解耦联蛋白3的调节机制  

The effects of oxidative stress induced by occlusal interference and the regulatory mechanism of UCP3 on masseter in rats

作　　者：吴东蕾 刘静 WU Donglei;LIU Jing(Department of Prosthodontics,College of Stomatology,Jinan University, China Guangzhou510632)

机构地区：[1]暨南大学口腔医学院口腔修复教研室,广州510632

出　　处：《实用口腔医学杂志》2019年第1期146-148,共3页Journal of Practical Stomatology

摘　　要：建立咬合干扰大鼠模型,建模后干扰侧咬肌组织MDA含量逐渐升高,而SOD、GPX活性则下降,UCP3表达水平升高(P <0. 05)。提示咬合干扰引起大鼠咬肌氧化应激损伤,而UCP3可能与氧化应激损伤机制调节相关。The occlusal interference model in rats was established. In the masseter the level of MDA was increased,but both SOD and GPX were decreased in the presence of the occlusal interference,while the expression of UCP3 was higher than that in the control group( P < 0. 05).The findings indicate that the occlusal interference can induce the oxidative damage of masseter in rats,which has a correlation with UCP3.

关 键 词：氧化应激 解偶联蛋白3 咬合干扰 

分 类 号：R783[医药卫生—口腔医学]