Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells
10.13422/j.cnki.syfjx.20191839
- VernacularTitle: 丁香脂素对谷氨酸钠诱导的SH-SY5Y细胞兴奋性损伤的保护作用
- Author:
Qiu-xia YAN
1
;
Yan-mei LI
2
;
Yan-hua FAN
2
;
Ming-sheng ZHANG
1
;
Li-shou YANG
2
;
Yao YAO
2
;
Jue YANG
2
;
Juan CHEN
2
;
Qun LONG
2
;
Jian-fei QIU
2
;
Xiao-sheng YANG
2
Author Information
1. School of Life Sciences, Guizhou University, Guiyang 550025, China
2. The Key Laboratory of Chemistry for Natural Products of Guizhou Province and Chinese Academy of Sciences, Guiyang 550014, China
- Publication Type:Research Article
- Keywords:
syringaresinol;
sodium glutamate;
nerve excitatory injury;
human neuroblastoma cell (SH-SY5Y);
neuroprotective effect
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(18):76-82
- CountryChina
- Language:Chinese
-
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 (P<0.01), ROS accumulation was significant (P<0.01), mitochondrial membrane potential was significantly decreased (P<0.01), and the expression of poly-ADP-ribose polymerase (PARP) and PARP1 protein was significantly decreased (P<0.01), the apoptotic rate of cells also increased significantly (P<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 (P<0.01), decreased ROS accumulation (P<0.01), restored mitochondrial membrane potential(P<0.01), up-regulated PARP, PARP1 protein (P<0.01), decreased apoptosis rate (P< 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.
