芍药苷对氯化钴诱导PC12细胞氧化应激损伤的保护作用

Protective effects of paeoniflorin on CoCl2-induced oxidative stress injury of PC12 cells

目的研究芍药苷对氯化钴诱导PC12细胞氧化应激损伤的保护作用。方法芍药苷预先处理PC12细胞1 h,再加入CoCl2共孵育24 h。采用MTT法检测PC12细胞存活率,利用DCFH-DA探针、Annexin FITC-V/PI双染法、JC1探针检测芍药苷(100、200μg/mL)对PC12细胞ROS水平、细胞凋亡率及线粒体膜电位值(MMP)的影响。结果CoCl2诱导PC12细胞24 h后,其半数抑制浓度(IC50)为1.2 mmol/L。与模型组比较,200μg/mL芍药苷提高CoCl2诱导PC12细胞存活率(P<0.05),减少细胞内ROS水平(P<0.05),抑制细胞凋亡(P<0.05),提高MMP(P<0.05)。结论芍药苷对CoCl2诱导PC12细胞氧化应激损伤有显著保护作用。

AIM To study the protective effects of paeoniflorin on CoCl2-induced oxidative stress injury of PC12 cells.METHODS PC12 cells previously subjected to 1h paeoniflorin pre-treatment were incubated with CoCl2 for 24 h in vitro.PC12 cells had their survival rate detected by MTT method;and their ROS level,cell apoptosis rate and mitochondrial membrane potential(MMP)due to the effect of paeoniflorin(100,200μg/mL)determined by the DCFH-DA probe,Annexin FITC-V/PI double staining method,and JC-1 probe.RESULTS The IC50 of PC12 cells was 1.2 mmol/L under 24 h CoCl2 induction..Compared with the model group,the group intervened with 200μg/mL paeoniflorin shared increased survival rate of CoCl2-induced PC12 cells(P<0.05),decreased intracellular ROS level(P<0.05),inhibited cell apoptosis(P<0.05),and increased MMP(P<0.05).CONCLUSION Paeoniflorin is significantly protective to CoCl2-induced oxidative stress injury of PC12 cells.