Protective effect of NIM811 on hypoxia/reoxygenation injury of hippocampal neurons in mice
10.19845/j.cnki.zfysjjbzz.2022.0023
- VernacularTitle:NIM811对Na2S2O4引起小鼠HT22细胞缺氧/复氧损伤的保护作用的研究
- Author:
Dan WANG
1
;
Chengjun ZHAO
1
;
Guisheng CHEN
1
Author Information
1. Clinical College of Ning Xia Medical University,Yinchuan 750004,China
- Publication Type:Journal Article
- Keywords:
NIM811;
Anoxia/reoxygenation;
Reactive oxygen species;
Mitochondrial membrane potential;
Calcium overload
- From:
Journal of Apoplexy and Nervous Diseases
2022;39(2):100-103
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and mechanism of the derivative NIM811 on hypoxia/reoxygenation injury of rat hippocampal neuron (HT22) induced by sodium disulfite (Na2S2O4).Methods The hypoxia/reoxygenation cell model was prepared with mouse HT22 cultured cells.The experiment was divided into normal control group,Na2S2O4 group,Na2S2O4+NIM811 group,and NIM811 group.Cell survival rate was detected by CCK-8,flow cytometry was used to detect apoptosis,mitochondrial membrane potential was detected by JC-1 reagent,calcium ion level in mitochondria was observed by Rhod-2 AM,and reactive oxygen species (ROS) was detected by DCFH-DA method.Results Compared with the Na2S2O4 group,after NIM811 treatment:(1)Cell activity increased by 38% (P<0.01);(2)Apoptosis decreased by 27% (P<0.01);(3)Mitochondrial membrane potential increased (P<0.01);(4)The level of calcium ions in the mitochondria decreased (P<0.01);(5)The level of reactive oxygen species (ROS) decreased (P<0.01).Conclusion NIM811 has a protective effect on the hypoxia/reoxygenation injury of mouse hippocampal neurons caused by Na2S2O4.The mechanism may be related to the maintenance of mitochondrial homeostasis and inhibition of cell apoptosis.NIM811 has therapeutic potential for future clinical treatment of ischemic stroke.
- Full text:2024072611240037988NIM811对Na2S2O4引起小鼠HT22细胞缺氧_复氧损伤的保护作用的研究.pdf
