| 黄芪甲苷对PC12细胞氧化应激损伤的保护作用 |
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| 引用本文： | 黄万刚,杨东风,冯佳良,黄淮,高超,徐正虎.黄芪甲苷对PC12细胞氧化应激损伤的保护作用[J].中国临床神经外科杂志,2021,26(4):270-273. |
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| 作者姓名： | 黄万刚 杨东风 冯佳良 黄淮 高超 徐正虎 |
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| 作者单位： | 065000 河北廊坊，河北中石油中心医院神经外科（黄万刚、冯佳良、高 超、徐正虎），急诊科（杨东风），神经内科（黄 淮） |
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| 基金项目： | 廊坊市科技支撑计划项目(2020013092)。 |
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| 摘 要： | 目的 探讨黄芪甲苷对PC12细胞氧化应激损伤的作用。方法 体外培养PC12细胞，6-羟基多巴胺（6-OHDA）作用PC12细胞导致氧化应激损伤。根据细胞作用方法随机分为4组:①对照组，采用完全培养基正常培养；②6-OHDA组，给予终浓度为100 μmol/L的6-OHDA处理24 h；③低、中、高剂量黄芪甲苷组，分别给予终浓度为25、50、100 μmol/L的黄芪甲苷预处理24 h，然后给予终浓度为100 μmol/L 6-OHDA处理24 h；④AG490组，以20 μmol/L AG490（JAK2/STAT3信号通路抑制剂）预处理16 h，加入终浓度为100 μmol/L黄芪甲苷处理24 h，然后再给予终浓度为100 μmol/L 6-OHDA处理24 h。CCK8法检测细胞生存率，流式细胞仪检测细胞凋亡率，酶联免疫吸附实验法检测细胞上清液超氧化物歧化酶（SOD）和丙二醛（MDA）水平，免疫印迹法检测细胞p-JAK2和p-STAT3蛋白表达。结果 6-OHDA作用后，PC12细胞存活率明显降低，细胞凋亡率明显升高，细胞培养液SOD水平明显降低、MDA水平明显升高，细胞p-JAK2和p-STAT3蛋白表达水平明显降低；黄芪甲苷预处理明显逆转6-OHDA的作用，而且呈剂量依赖性；AG490预处理明显逆转黄芪甲苷的作用。结论 6-OHDA作用PC12细胞，可导致氧化应激损伤促使细胞凋亡；黄芪甲苷预处理能激活JAK2/STAT3信号通路，抑制6-OHDA对PC12细胞的损伤，对PC12细胞起保护作用。
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| 关 键 词： | 黄芪甲苷 6-羟基多巴胺 PC12细胞 JAK2/STAT3信号通路 氧化应激损伤 |
Protective effect of astragalosideⅣon 6-OHDA-induced oxidative stress injury in PC12 cells via activation of JAK2/STAT3 signaling pathway |
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| HUANG Wan-gang,YANG Dong-feng,FENG Jia-liang,HUANG Huai,GAO Chao,XU Zheng-hu.Protective effect of astragalosideⅣon 6-OHDA-induced oxidative stress injury in PC12 cells via activation of JAK2/STAT3 signaling pathway[J].Chinese Journal of Clinical Neurosurgery,2021,26(4):270-273. |
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| Authors: | HUANG Wan-gang YANG Dong-feng FENG Jia-liang HUANG Huai GAO Chao XU Zheng-hu |
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| Affiliation: | 1. Department of Neurosurgery, Hebei Petro China Central Hospital, Langfang 065000, China; 2. Department of EmergencyHebei Petro China Central Hospital, Langfang 065000, China; 3. Department of Neurology, Hebei Petro China Central Hospital, Langfang 065000, China |
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| Abstract: | Objective To investigate the effect of astragiosideⅣ(ASⅣ)on the 6-hydroxydopamine(6-OHDA)-induced oxidative stress injury in PC12 cells.Methods PC12 cells were cultured in vitro and the 6-hydroxy dicamine(6-OHDA)was used to cause oxidative stress injury in the PC12 cells.The PC12 cells were randomly divided into 4 groups:①control group,the PC12 cells were cultured in medium without any drugs;②6-OHDA group,the PC12 cells were treated by 6-OHDA for 24 h at a final concentration of 100μmol/L;③low,medium,and high dose ASⅣgroups,the PC12 cells were treated by ASⅣfor 24 h at a final concentration of 25,50,100μmol/L,respectively,and then treated by 6-OHDA for 24 h;④Ag490 group,the PC12 cells were trated by AG490(JAK2/STAT3 signaling inhibitor)for 16 h at a final concentration of 20μmol/L,then treated by ASⅣfor 24 h at a final concentration of 100μmol/L,and finally treated by 6-OHDA for 24 h.CCK8 method was used to detect the cell survival rate.Cytometry was used to detect the cell apoptosis rate.Enzyme-linked immunosorbent assay was used to detect the cell supernatant levels of superoxide dismutase(SOD)and malondialdehyde(MDA).Western blotting was used to detect the protein expression levels of p-JAK2 and p-STAT3.Results After 6-OHDA treatment,the survival rate of PC12 cells significantly reduced,and the apoptosis rate significantly increased,the SOD level in cell culture medium significantly reduced,the MDA level significantly increased,and the expression levels of p-JAK2 and p-STAT3 protein significantly reduced.ASⅣpretreatment significantly reversed the effect of 6-OHDA on the PC12 cellsdose-dependent manner.AG490 pretreatment significantly reversed the effect of ASⅣ.Conclusions 6-OHDA treatment can result in oxidative stress injury in PC12 cells and then cause cell apoptosis in PC12 cells.ASⅣpretreatment can significantly inhibit the 6-OHDA-induced damage to PC12 cells by activating JAK2/STAT3 signaling pathways. |
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| Keywords: | AstragalosideⅣ 6-hydroxydopamine(6-OHDA) PC12 cell JAK2/STAT3 signaling pathway Oxidative stress |
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