Superoxide dismutase 2 mediates the protective effect of berberine on neuronal damage induced by oxygen-glucose deprivation in HT22 mouse hippocampal neuronal cell
10.3760/cma.j.issn.1673-4165.2019.05.007
- VernacularTitle:超氧化物歧化酶2介导小檗碱对氧-葡萄糖剥夺复氧复糖所致HT22小鼠神经元损伤的保护作用
- Author:
Xilong ZHANG
1
;
Xiaoyan LIU
;
Hui CHENG
;
Wanfang XIONG
;
Ji JIA
;
Yuanyuan ZHANG
Author Information
1. 西安市酃邑区妇幼保健院麻醉科 710300
- Keywords:
Neurons;
Apoptosis;
Berberine;
Superoxide dismutase;
Oxidative stress;
Oxygen;
Glucose;
Reperfusion injury;
Neuroprotection;
Models,biological
- From:
International Journal of Cerebrovascular Diseases
2019;27(5):355-362
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of berberine (BBR) on neuronal damage induced by oxygen-glucose deprivation (ODD) in HT22 mouse hippocampal neuronal cell,and the role of superoxide dismutase 2 (SOD2) in it.Methods HT22 cells were exposed to OGD for 4 h and then reoxygenated for 24 h to simulate ischemia-reperfusion injury.The HT22 cells were divided into control group,OGD group,BBR + OGD group,SOD2-siRNA + BBR + OGD group,and scrambled (SC)-siRNA + BBR + OGD group.Cell viability was measured by thiazole blue method.Cell morphology was observed by phase contrast microscopy.Medium lactate dehydrogenase (LDH) level,intracellular glutathione (GSH),and catalase (CAT) content were detected by colorimetric assay.The cell apoptosis rate was detected by flow cytometry.The expression level of cleaved caspase-3 was detected by Western blot analysis.Results Compared with the control group,OGD significantly decreased cell viability,intracellular GSH,and CAT level (all P ＜0.05),increased cell LDH release,apoptosis rate,and cleaved caspase-3 protein expression level (all P＜0.05).At the same time,cell morphology destruction was observed.BBR significantly reduced the above damage of HT22 cells induced by OGD (all P ＜0.05),while SOD2-siRNA significantly reversed the protective effect of BBR on HT22 cells (all P ＜0.05).Conclusions BBR significantly alleviated neuronal damage induced by recovery of oxygen-glucose after OGD.SOD2 might mediate its protective effect.
