活性维生素D在调节髁突软骨细胞氧化应激水平中的作用

The effect of 1,25(OH)_2D_3 in regulating of the level of oxidative stress in temporomandibular joint condylar chondrocyte

目的:通过构建活性维生素D缺乏的髁突软骨细胞氧化应激模型,探讨活性维生素D在颞下颌关节骨关节病发生中的作用。方法:给予外源性过氧化氢(H_2O_2)刺激,以构建SD大鼠髁突软骨细胞氧化应激模型,通过慢病毒转染敲低软骨细胞维生素D受体(VDR),构建SD大鼠软骨细胞活性维生素D缺乏模型。用H_2O_2刺激维生素D缺乏SD大鼠软骨细胞,以诱导氧化应激水平增高,继而加入外源性活性维生素D,比较各组间氧化应激水平及相关生化指标丙二醛(MDA)、总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-px)的变化。结果:活性维生素D缺乏的软骨细胞受到外源性H_2O_2刺激后,其氧化应激水平较对照组明显增高,相关标记物活性变化亦呈现此趋势,加入外源性1,25(OH)_2D_3后两组细胞氧化应激水平均明显下调,而实验组氧化应激水平仍明显高于对照组。结论:活性维生素D的缺乏可导致髁突软骨细胞氧化应激水平增高。

Objective:To discuss the effect of 1,25(OH)2 D 3 in regulation of the level of oxidative stress in temporomandibular joint chondrocyte by constructing the model of 1,25(OH)2 D 3 deficiency chondrocyte in oxidative stress state.Methods:Knocking down the level of vitamin D receptor in the temporomandibular joint condylar chondrocytes of SD rats by lentivirus infection in order to simulate the 1,25(OH)2 D 3 deficiency status.Using the exogenous hydrogen peroxide to stimulate both the normal and 1,25(OH)2 D 3 deficiency chondrocytes we established the oxidative stress model in vitro.Detecting the alteration of oxidative stress level in both groups after being treated with exogenous 1,25(OH)2 D 3.Malonaldehyde,total superoxide dismutase,Glutathione peroxidase and reactive species oxygen in each group were detected and compared as representing the oxidative stress level in each group.Results:The oxidation level was increased in 1,25(OH)2 D 3 deficiency chondrocytes after being treated with hydrogen peroxide.Treated with 1,25(OH)2 D 3,the level of oxidative stress were decreased obviously in both the normal and 1,25(OH)2D 3 deficiency chondrocytes.However the level of oxidative stress in 1,25(OH)2 D 3 deficiency chondrocytes was still fairly higher than that of the normal group.Conclusions:The deficiency of 1,25(OH)2 D 3 can increase the level of oxidative stress.