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芍药苷对氯化钴诱导PC12细胞氧化应激损伤的保护作用 被引量:6

Protective effects of paeoniflorin on CoCl2-induced oxidative stress injury of PC12 cells
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摘要 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.
作者 雷昌 黄丹 向韵 张秀丽 孟盼 邹蔓姝 王宇红 凌成利 LEI Chang;HUANG Dan;XIANG Yun;ZHANG Xiu-li;MENG Pan;ZHOU Man-shu;WANG Yu-hong;LING Cheng-li(Training Bases of Hunan Province&National Ministry Co-founded Key Laboratory for Chinese Materia Medica Powder and Innovative Drugs,Hunan University of Traditional Chinese Medicine,Changsha 410208,China;Science and Technology Innovation Center,Hunan University of Traditional Chinese Medicine,Changsha 410208,China)
出处 《中成药》 CAS CSCD 北大核心 2020年第10期2605-2610,共6页 Chinese Traditional Patent Medicine
基金 湖南中医药大学中医学国内一流建设学科资助项目(2018) 湖南中医药大学中医学一级学科开放性基金项目(2018ZYX48)。
关键词 芍药苷 脑卒中 氧化应激 凋亡 paeoniflorin ischima stroke oxidative stress apoptosis
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