Hippocampal astrocytes in juvenile rats with persistent epilepsy: The role of cannabinoid receptor type 2 in regulating MAPK pathway
10.3969/j.issn.2095-4344.2868
- Author:
Qing Jun CAO
1
Author Information
1. Department of Pediatric Neurology, Shengjing Hospital of China Medical University
- Publication Type:Journal Article
- Keywords:
Astrocytes;
Cannabinoid receptor type 2;
Experiment;
Juvenile rats;
MAPK pathway;
Status epilepticus
- From:
Chinese Journal of Tissue Engineering Research
2020;24(32):5179-5185
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Astrocyte proliferation is an important morphological change in epilepsy. Proliferated glial cells can produce cytokines, and in turn activates JAK/STAT signal transduction to promote glial cell proliferation, which affects the occurrence and recurrence of epilepsy. Astrocytes and signal transduction pathways interact with each other to play a role in the pathogenesis of epilepsy. OBJECTIVE: To investigate the effect of cannabinoid receptor type 2 (CB2R) on the activation of ERK, p38, and JNK proteins in astrocytes and MAPK pathways in juvenile rats with persistent epilepsy. METHODS: Forty healthy male Sprague-Dawley rats (18-21 days old) were randomly divided into four groups: normal control group, epilepsy model group, CB2R agonist JWH133 group, CB2R antagonist AM630 group. The normal control group was given only normal saline. In the other groups, rats were intraperitoneally injected with lithium chloride and pilocarpine to establish epilepsy models, and different interventions were performed. Twenty-four hours after the onset of epilepsy, brain tissues were taken. Co-expression of GFAP and p-ERK, p-p38, and p-JNK in hippocampal tissue was detected by immunofluorescence. Real-time PCR was used to detect the expression of GFAP mRNA in hippocampal tissue. RESULTS AND CONCLUSION: The co-expression of GFAP/p-ERK and GFAP/p-p38 was significantly higher in the epilepsy model group than the normal control group (P < 0.05), significantly lower in the JWH133 group than the epilepsy model group (P < 0.05), and significantly higher in the AM630 group than the JWH133 group (P < 0.05). The co-expression of GFAP/p-JNK was significantly lower in the epilepsy model group than in normal control group (P < 0.05), significantly higher in the JWH133 group than the epilepsy model group (P < 0.05), and significantly lower in the AM630 group than the JWH133 group (P < 0.05). The mRNA expression of GFAP was significantly decreased in the epilepsy model group compared with the normal control group (P < 0.05), significantly increased in the JWH133 group compared with the epilepsy model group (P < 0.05), and significantly reduced in the AM630 group compared with the JWH133 group (P < 0.05). Therefore, CB2R can regulate the expression of ERK, p38, JNK proteins in the MAPK pathway, thereby affecting astrocytes in the hippocampus of juvenile rats with persistent epilepsy.
