Compound brain peptide gangiioside can improve intrauterine hypoxia-induced neonatal brain injury and promote synapse regeneration in a mouse model
10.3969/j.issn.2095-4344.2478
- Author:
Fuhua ZHANG
1
Author Information
1. Department of Traditional Chinese Medicine, Luohe Medical College
- Publication Type:Journal Article
- Keywords:
Brain injury;
Collagen IV;
Compound porcine cerebroside and gangiioside injection;
Intrauterine hypoxia;
Scientific and Technological Breakthrough Foundation of Henan Province
- From:
Chinese Journal of Tissue Engineering Research
2020;24(11):1689-1694
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: The most current application of compound porcine cerebroside and gangiioside injection (CPCGI) focuses on the clinical therapeutic efficacy in some craniocerebral injuries and neonatal hypoxic ischemic encephalopathy, but the molecular mechanism of CPCGI involved in the recovery of nerve function is rarely reported. OBJECTIVE: To study the protective effect and mechanism of CPCGI in a neonatal mouse model of intrauterine hypoxia-induced brain injury. METHODS: Fifteen Kunming mice were randomly divided into control group, hypoxia group and treatment group. At the 14th day after pregnancy, mice in hypoxia group and treatment group were put into a 10% oxygen incubator to make the model of intrauterine hypoxia. After delivery, neonatal mice were intraperitoneally injected with CPCGI and PBS respectively, and mouse development in each group was observed after treatment. Mice in the control group were not hypoxic and treated. The expression of glial fibrillary acidic protein, Neurocan, SynDIGI and collagen IV were observed by immunofluorescence staining and western blot assay. A step-down test was used to test animal memory function. The study protocol was approved by the Animal Ethic Committee of Luohe Medical College in China. RESULTS AND CONCLUSION: Compared with the control group, the expressions of glial fibrillary acidic protein and Neurocan in the hypoxia group were significantly increased, while the expressions of SynDIGI and collagen IV were significantly decreased. The expression of SynDIGI and collagen IV in the treatment group was significantly increased than that in the hypoxia group, while the expression of glial fibrillary acidic protein and Neuroncan was significantly decreased than that in the hypoxia group. The learning and memory ability of mice in the hypoxia group was significantly decreased compared with the control group, but was significantly improved after CPCGI treatment. These results suggest that CPCGI can alleviate brain injury and improve learning and memory ability after hypoxic ischemic encephalopathy. The detailed mechanism might be related to inhibiting activation of astrocytes, down-regulating Neuroncan expression, up-regulating collagen IV expression, promoting synaptic reconstruction and reducing cerebrovascular injury.
