Expression of immune molecules in epileptogenic rats
- VernacularTitle:实验性癫痫大鼠免疫分子的表达
- Author:
Changqian ZENG
;
Jinyan WANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2006;10(14):188-189,192
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: The relation of epilepsy to immunity has been investigated at cellular and molecular levels in recent years, and the results show many immunological changes in epileptic patients such as immunocytes,immune molecules and immune functions.OBJECTIVE: To investigate the immunologic pathogenesis of epilepsy and expression of MHC- Ⅰ, MHC- Ⅱ and C3b receptor of microglia. DESIGN: Randomized and controlled trial. SETTING: Medical College of Dalian University; University of Sanchong,Japan.MATERIALS: The experiment was conducted in the Immunology Laboratory of Jilin Beihua University from 2001 to 2002. Forty adult Wistar rats were randomized into model group and control group with 20 in each group.METHODS: 12 mg/kg kainic acid was administered subcutaneously into rats in model group, while no intervention was given to rats in control group. Seizure was observed within 6 hours following kainic acid administration. Rats were killed 3 days after medication. Neuronal degeneration was observed with crystal violet staining and the expression of MHC molecules and C3b receptor in the hippocampus of epileptogenic rats was observed immunnhistochemically.administration, spasm occurred within 3 hours after kainic acid administration and continued from the first stage to the fifth stage. More severe served in cone-like cell layer of hippocampus of rats in model group, but molecule, MHC- Ⅱ molecule and C3b receptor was (201.6±6.43), (493.8±7.92) and (362.5±3.18) cells per visual field respectively in the hippocampus of epileptogenic rats inmodel group, but no obvious expression was observed in control group. The differences were significant between the two groups (P ＜ 0.01).pocampal sclerosis, immunological inflammation is observed combined with the complement system, which indicates immunologic inflammatory mechanism of epilepsy.
