Relationship between the hippocampal activin beta-A subgene expression and the endogenous protective effects of neurons on antagonizing excitatory injury
- VernacularTitle:海马活化素βA亚基基因表达与神经元对抗兴奋性损害内源性保护效应的关系
- Author:
Juming YU
;
Deben YANG
;
Huimin REN
;
Yuping JIANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2005;9(9):222-225
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Since the discovery of the fact that activin can promote the survival of retinal neurocyte in chicken,the effects of activin in nervous system receives recognition. As discovered recently,hippocampal activin βA mRNA expression up-regulates in multiple brain injury animal models including ischemia and hypoxia; however,the change of activin βA mRNA expression after epilepsy is waiting for investigation.OBJECTIVE: To observe hippocampal activin βA mRNA expression at different time point after pilocarpine (PC) -induced epilepsy in mouse to explore its mechanism.DESIGN: A randomized controlled experimental study based on the experimental animals.SETTING: Department of neurology in a university affiliated hospital and the institute of neurology in a university.MATERIALS: The study was conducted in the Institute of Neurology of Huashan Hospital Affiliated to Fudan University and the Department of Pathology of Shanghai Medical College between November 2001 and July 2002. Totally 168 eight to ten-week old healthy male C57BL/6 mice with a body mass between 20 g and 25 g were obtained from Shanghai Experimental Animal Center,Chinese Academy of Science.INTERVENTIONS: 350 mg/kg(10 g/L) of PC was injected into the abdominal cavity in the mice of study group,in which 1 mg/kg of scopolamine (SC) was injected at 30 minutes before the injection of PC to antagonize its peripheral cholinergic reaction. Status epilepticus(SE) model mouse was the mouse with continuous mgoelonus or generalized seizure of rigid clonus that lasted for 1 hour after the injection of PC. Valium(4 mg/kg) was immediately injected after the modeling to terminate seizure. Same dose of Valium was injected into non-SE(NSE) mice after 1.5 hours of PC injection. Saline was used to replace PC to inject into mice of control group,and the rest disposals of control group were as same as that of study group. SE mice,NSE mice and control mice were randomly divided into six subgroups including 0hour,1 hour,3 hours,6 hours,24 hours and 48 hours subgroups according to the time point after modeling with 6 mice of each subgroup(mice of NSE group and subgroups of 0 hour time point were not included into analysis of hybridization in situ).MAIN OUTCOME MEASURES: Hippocampal activin βA mRNA expression of different time point in SE mice and NSE mice were observed by RT-PCR; the distribution of hippocampal activin βA mRNA expression at different time points in mice were observed by hybridization in situ.RESULTS: There was no significant change of hippocampal activin βA mRNA expression at different time point in mice of NSE group and control group. In SE group,activin βA mRNA(0.49 ± 0. 11) had a transient significant decrease at the beginning(0 hour),which rapidly returned to control level(0. 74 ±0. 13) at 1 hour(0.73 ±0. 12) . Activin βA mRNA continuously increased and reached (0.97 ±0. 24) at 3 hours,(1.34 ±0. 19) at 6 hours,maintained (0.98 ±0. 17) until 24 hours,and decreased to (0. 83 ± 0.09) at 48 hours afterwards,which was slightly higher than control level. Compared with control group,the increases at 3 hours,6 hours and 24hours were significant( t = 2. 668,6. 289,2. 916,P ＜ 0. 001 - 0. 05). The significant up-regulation of activin βA mRNA expression was occurred earliest in hippocampal CA2 and DG regions at 3 hours after SE,and the significant expressions also could be seen in CA3 region after 6 hours. There were expressions in only CA2 and CA3 regions after 24 hours,while there were very few positive cells in CA2 region after 48 hours.CONCLUSION: PC-induced SE could significantly up-regulate hippocampal activin βA mRNA expression,while NSE has no such up-regulative effect. The up-regulation of hippocampal activin βA mRNA expression might be an endogenous protective effect of neuron on antagonizing excitatory injury.
