ABSTRACT
Objective To explore the effect of the exogenous phosphorylation cyclic adenosine monophosphate response element bind-ing protein (pCREB) antibody on the expression of apoptotic regulated genes (Bcl-2 and c-Jun) in hippocampus after status convulsivus (SC), to elucidate the role and regulation mechanism of pCREB in convulsive brain injury. Methods Seizures were induced in 24 adult Wi-star rats with lithium-pilocarpine intraperitoneal injection (SC group), another 24 rats were as the normal controls (NC group). Each group was divided into no injection subgroup, normal saline injection subgroup and anti pCREB subgroup according to the injection contents of lat-eral ventricle, with 8 cases in each group. They were sacrificed 6 hours after injection. Both the protein and mRNA expression of Bcl-2 and c-Jun in bilateral hippocampus were detected by immunohistochemistry and in situ hybridization, respectively. Results There was no signifi-cant difference in Bcl-2 protein/mRNA expression among 3 subgroups in the NC group (P>0.05). In the SC group, the expression of Bcl-2 protein/mRNA were lower in the anti pCREB subgroup than in the no injection subgroup and normal saline injection subgroup (P<0.05). There was significant difference in c-Jun protein/mRNA expression among 3 subgroups in both NC group and SC group (P<0.001). The ex-pression of c-Jun protein/mRNA was higher in the normal saline injection subgroup and the anti pCREB subgroup than in the no injection group (P<0.05), especially in the anti pCREB subgroup (P<0.05). Conclusion Exogenous anti-pCREB antibody can down-regulate the ex-pression of Bcl-2 and up-regulate the expression of c-Jun in hippocampal cells after SC.
ABSTRACT
@#ObjectiveTo explore the influences of age and duration of status convulsivus （SC） on mitochondrial membrane potential (△Ψm） in hippocampus. MethodsConvulsive seizures for 30 min or 3 h (30 min SC or 3 h SC) were induced in 80 infant (20 d after birth) and 80 adult Wistar rats (IRs ＆ ARs respectively) with lithium-pilocarpine ip. The rats were sacrificed at 6 different time points from the 3rd hour to 7th day after SC termination. The mitochondrial △Ψm in hippocampal cells was determined with flow cytometry. ResultsThe mitochondrial △Ψm in hippocampal cells started to decrease at the 3th hour after SC in both IRs and ARs. The bottom level was reached at the 6th hour after SC ［(6.08±0.43) in IRs and (5.70±0.63) in ARs ) ］. Both of them were significantly lower than that of control group (P<0.01） and began to increase at 12th hour after SC. On the 7th day after 30 minutes SC, the level of mitochondrial △Ψm in IRs increased to the level of control, while the level in ARs was still lower than that of control (P<0.05）. At the 3rd hour, the 3rd and the 7th day after SC, the levels of mitochondrial △Ψm in IRs were obviously higher than those in ARs. Compared with the same time point after 30 min SC, the levels of mitochondrial △Ψm at the 3rd and the 6th hour after 3 h SC were much lower in different age groups (P<0.05）. Except the effect of the age-related difference, there was a positive correlation between the duration of SC and the changes of mitochondrial △Ψm in partial correlation analysis （r=0.71，P<0.05）. ConclusionSevere seizure could induce the mitochondrial △Ψm decreased in hippocampus. Age and duration of SC were important factors associated with the mitochondrial △Ψm decrease. There may be an internal protective response against brain damage in premature brain.
