摘要
目的探讨白藜芦醇(Res)对H_2O_2诱导的THP-1源性巨噬细胞氧化损伤的影响。方法采用H_2O_2处理培养THP-1源性巨噬细胞,造成氧化应激模型。不同终度的Res预作用THP-1源性巨噬细胞组1 h后加入300μmol/L H_2O_2作用24 h。应用MTT比色法检测细胞存活率,黄嘌呤氧化法检测超氧化物歧化酶(SOD)的活力,硫代巴比妥酸比色法检测丙二醛(MDA)含量。结果与空白对照组比较,不同浓度H_2O_2处理THP-1源性巨噬细胞24 h后,THP-1源性巨噬细胞的存活率呈剂量依赖性下降(P<0.05)。Res预处理组的细胞存活率均高于模型组(300μmol/L H_2O_2)(P<0.05),且以40μmol/L Res作用效果最佳。40~100μmol/L Res预处理组与模型组相比,MDA的含量明显减少,SOD的活力升高(P<0.05)。结论 Res可减轻H_2O_2对THP-1源性巨噬细胞的损伤程度,其机制可能与其抗氧化作用有关。
Objective To investigate the effect of resveratrol (Res) on hydrogen peroxide (H2O2) -induced oxidative stress in THP-1 macrophages. Methods The oxidative model was induced by H2O2 stimulation. THP-1 macrophages were pretreated with different concentrations of Res for 1 h and then treated with H2O2 ( 300 μmol/L) for 24 h. The viability of macrophages was measured by MTT assay. The SOD activity was assayed by using xanthine oxidase method. Thiobarbituric acid colorimetric approach was employed to determine the level of MDA. Results Compared with the normal control group, treatment with H202 decreased the cell viability (P〈0.05). Compared with the model group, the survival rate of cells was significantly increased in Res-pretreated group, especially when Res at 40 μmol/L. Meantime, Res at 40- 100 μmol/L reduced the level of MDA and increased the activity of SOD (P〈0.05). Conclusion Res can mitigate the oxidative injury of macrophages induced by H202, which may be related to its ant/oxidant effect.
出处
《广东药科大学学报》
CAS
2017年第2期203-206,共4页
Journal of Guangdong Pharmaceutical University
基金
广东省自然基金面上项目(2016A030313755)