[1]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(04):270-273.[doi:10.13798/j.issn.1009-153X.2021.04.014]
 HUANG Wan-gang,YANG Dong-feng,FENG Jia-liang,et al.Protective effect of astragaloside Ⅳ on 6-OHDA-induced oxidative stress injury in PC12 cells via activation of JAK2/STAT3 signaling pathway[J].,2021,26(04):270-273.[doi:10.13798/j.issn.1009-153X.2021.04.014]
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黄芪甲苷对PC12细胞氧化应激损伤的保护作用()
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《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
26
期数:
2021年04期
页码:
270-273
栏目:
实验研究
出版日期:
2021-04-25

文章信息/Info

Title:
Protective effect of astragaloside Ⅳ on 6-OHDA-induced oxidative stress injury in PC12 cells via activation of JAK2/STAT3 signaling pathway
文章编号:
1009-153X(2021)04-0270-04
作者:
黄万刚 杨东风 冯佳良 黄 淮 高 超 徐正虎
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)
Author(s):
HUANG Wan-gang1 YANG Dong-feng2 FENG Jia-liang1 HUANG Huai3 GAO Chao1 XU Zheng-hu1.
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
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
Keywords:
Astragaloside Ⅳ 6-hydroxydopamine (6-OHDA) PC12 cell JAK2/STAT3 signaling pathway Oxidative stress
分类号:
R 742.5
DOI:
10.13798/j.issn.1009-153X.2021.04.014
文献标志码:
A
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。
Abstract:
Objective To investigate the effect of astragioside Ⅳ (AS Ⅳ) 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 100 μmol/L; ③low, medium, and high dose AS Ⅳ groups, the PC12 cells were treated by AS Ⅳ for 24 h at a final concentration of 25, 50, 100 μmol/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 20 μmol/L, then treated by AS Ⅳ for 24 h at a final concentration of 100 μmol/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. AS Ⅳ pretreatment significantly reversed the effect of 6-OHDA on the PC12 cellsdose-dependent manner. AG490 pretreatment significantly reversed the effect of AS Ⅳ. Conclusions 6-OHDA treatment can result in oxidative stress injury in PC12 cells and then cause cell apoptosis in PC12 cells. AS Ⅳ pretreatment can significantly inhibit the 6-OHDA-induced damage to PC12 cells by activating JAK2 / STAT3 signaling pathways.

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备注/Memo

备注/Memo:
基金项目:廊坊市科技支撑计划项目(2020013092)
通讯作者:徐正虎,E-mail:15547662276@163.com
更新日期/Last Update: 2021-04-25