Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells

Qiu-xia YAN; Yan-mei LI; Yan-hua FAN; Ming-sheng ZHANG; Li-shou YANG; Yao YAO; Jue YANG; Juan CHEN; Qun LONG; Jian-fei QIU; Xiao-sheng YANG

doi:10.13422/j.cnki.syfjx.20191839

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Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells

Pharmacology | 更新时间：2021-02-09

- Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 18, Pages: 76-82(2019)
- 作者机构：
  
  1.贵州大学　生命科学院，贵阳　 550025；
  2.贵州省中国科学学院　天然产物化学重点实验室，贵阳　 550014
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191839
  CLC： R2-0; R285.5; R289; R322.8
- Published：20 September 2019，
  
  Published Online：04 June 2019，
  
  Received：14 March 2019，
- 稿件说明：
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Qiu-xia YAN, Yan-mei LI, Yan-hua FAN, et al. Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells. [J]. Chinese Journal of Experimental Traditional Medical Formulae 25(18):76-82(2019)
DOI：

Qiu-xia YAN, Yan-mei LI, Yan-hua FAN, et al. Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells. [J]. Chinese Journal of Experimental Traditional Medical Formulae 25(18):76-82(2019) DOI： 10.13422/j.cnki.syfjx.20191839.

摘要

目的：

基于谷氨酸钠诱导人神经母细胞瘤细胞(SH-SY5Y)细胞损伤构建的模型，观察从枫香槲寄生中提取得到丁香脂素的保护，并探讨其作用机制。

方法：

采用谷氨酸钠构建SH-SY5Y细胞损伤模型，实验分为正常组，损伤模型组(谷氨酸钠50 mmol·L

－1

，谷氨酸钠50 mmol·L

－1

＋DMSO)，丁香脂素组(6.25，12.5，25 μmol·L

－1

)，通过细胞计数法，细胞形态学观察，Annexin V-FITC/碘化丙啶(PI)细胞凋亡检测、活性氧(ROS)检测、线粒体膜电位以及蛋白免疫印迹法(Western blot)等方法，评价丁香脂素对谷氨酸钠诱导的神经兴奋性损伤的神经保护活性。

结果：

与正常组比较，模型组的细胞存活率明显降低(

0.01)，ROS显著升高(

0.01)，线粒体膜电位显著降低(

0.01)，聚腺苷二磷酸-核糖聚合酶(PARP)，PARP1蛋白表达显著降低(

0.01)，细胞的凋亡率显著增大(

0.01)；与模型组比较，丁香脂素组(6.25，12.5，25 μmol·L

－1

)呈浓度依赖性增加细胞的存活率(

0.01)，减少ROS的积累(

0.01)，显著恢复线粒体膜电位的变化(

0.01)，显著上调PARP，PARP1蛋白(

0.01)，显著降低细胞凋亡率(

0.01)。

结论：

提示丁香脂素对谷氨酸钠诱导的SH-SY5Y神经细胞的兴奋性损伤具有显著的保护活性，其作用机制可能是通过抗氧化应激，修复线粒体功能及DNA损伤等通路来显著降低谷氨酸钠诱导的神经细胞凋亡。

Abstract

Objective:

To establish a model for the injury of human neuroblastoma cell (SH-SY5Y) induced by sodium glutamate

and to observe the protective effect of syringaresinol on cell damage from

Viscum liquidambaricolum

hayataon

and to explore its mechanism.

Method:

Construction of SH-SY5Y cell injury model using sodium glutamate.The experiment was divided into normal cell group

injury model group (sodium glutamate 50 mmol·L

-1

sodium glutamate 50 mmol·L

-1

+ DMSO)

syringaresinol experimental group (6.25

12.5

25 μmol·L

-1

)

by cell counting

cell morphology observation

Annexin V-FITC/PI apoptosis detection

ROS reactive oxygen species detection

mitochondrial membrane potential

and Western blot

evaluation of syringaresinol on glutamate-induced neuronal excitability injury neuroprotective activity.

Result:

Compared with normal group

the cell survival rate of the model group was significantly decreased (

0.01)

ROS accumulation was significant (

0.01)

mitochondrial membrane potential was significantly decreased (

0.01)

and the expression of poly-ADP-ribose polymerase (PARP) and PARP1 protein was significantly decreased (

0.01)

the apoptotic rate of cells also increased significantly (

0.01). Compared with the model group

the syringaresinol group (6.25

12.5

25 μmol·L

-1

) showed a concentration-dependent increase in cells. Survival rate (

0.01)

decreased ROS accumulation (

0.01)

restored mitochondrial membrane potential(

0.01)

up-regulated PARP

PARP1 protein (

0.01)

decreased apoptosis rate (

0.01).

Conclusion:

Syringaresinol has significant protective activity against excitatory damage induced by sodium glutamate in SH-SY5Y neurons

the mechanism may be through anti-oxidative stress

repairing mitochondrial function and DNA damage to significantly reduce sodium glutamate-induced neuronal apoptosis.

关键词

丁香脂素谷氨酸钠神经兴奋性损伤人神经母细胞瘤细胞(SH-SY5Y)神经保护作用

Keywords

syringaresinolsodium glutamatenerve excitatory injuryhuman neuroblastoma cell (SH-SY5Y)neuroprotective effect

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