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

摘要

Objective: To discuss the effect of 1,25(OH)2D3 in regulation of the level of oxidative stress in temporomandibular joint chondrocyte by constructing the model of 1,25(OH)2D3 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)2D3 deficiency status.Using the exogenous hydrogen peroxide to stimulate both the normal and 1,25(OH)2D3 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)2D3.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 oxida-tion level was increased in 1,25(OH)2D3 deficiency chondrocytes after being treated with hydrogen peroxide.Treated with 1,25(OH)2 D3,the level of oxidative stress were decreased obviously in both the normal and 1,25(OH)2D3 deficiency chondrocytes.However the level of oxidative stress in 1,25(OH)2D3 deficiency chondrocytes was still fairly higher than that of the normal group.Conclusions:The deficiency of 1,25(OH)2D3 can increase the level of oxidative stress.%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(H2O2)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H2O2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H2O2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)2D3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.