Time-dependent injury of mouse cerebral cortex and hippocampus by acute hypoxia.
- Author:
Hua-Xiang SHI
1
;
Meng-Wei ZHOU
2
;
Hu ZHOU
2
;
Jing-Xin ZHANG
2
;
Wei-Guo SHI
2
;
Li-Yun WANG
3
Author Information
1. School of Chemical Engineering and Technology, Tianjin University, Tianjin 300350, China.
2. State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Toxicology and Pharmacology, Academy of Military Medicine Sciences, Academy of Military Sciences, Beijing 100850, China.
3. State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Toxicology and Pharmacology, Academy of Military Medicine Sciences, Academy of Military Sciences, Beijing 100850, China. huaxiang_s0510@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Cerebral Cortex/metabolism*;
Hippocampus/metabolism*;
Hypoxia;
Malondialdehyde;
Mice;
Oxidative Stress;
Superoxide Dismutase/pharmacology*
- From:
Acta Physiologica Sinica
2022;74(2):145-154
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the harmful effects of acute hypoxia on mouse cerebral cortex and hippocampus and the underlying mechanism. Mouse model of acute hypoxia was constructed by using a sealed glass jar. Laser speckle contrast imaging was used to detect the changes of cerebral blood flow after different time duration of hypoxia. Total superoxide dismutase (T-SOD) and malondialdehyde (MDA) assay kits were used to detect oxidative stress in cerebral cortex and hippocampus. Immunofluorescent staining was used to detect neuroinflammatory response of microglia in the cerebral cortex and hippocampus. One-step TUNEL method was used to detect neuronal apoptosis. The results showed that, compared with non-hypoxia (0 min hypoxia) group, 30 min hypoxia group exhibited decreased cerebral blood flow, higher percentage of CD68+/Iba1+ microglia, and increased neural apoptosis in the cerebral cortex and hippocampus. Compared with 30 min group, 60 min hypoxia group showed significantly decreased cerebral blood flow, increased MDA content in the cortex, as well as greater percentage of CD68+/Iba1+ microglia and neuronal apoptosis in the cerebral cortex and hippocampus. These results suggest that acute hypoxia damages brain tissue in a time-dependent manner and the oxidative stress and neuroinflammation are important mechanisms.
