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Expressions of Endoplasmic Reticulum Stress-Related Factors CCAAT/Enhancer-Binding Protei-Homologous Protein and Caspase-12 in Epileptic Brain Damage in Rats Induced by Lithium-Pilocarpine and Effect of Erythropoietin on Their Expression

YUAN Yan,JIA Tian-ming,LI Xiao-li,YIN Xing(Department of Pediatrics,the Third Affiliated Hospital of Zhengzhou University,Zhengzhou 450052,Henan Province,China)  
Objective To observe the endoplasmic reticulum stress-related factors CCAAT/enhancer-binding protei-homologous protein(CHOP),Caspase-12 expression in hippocampus and explore possible mechanism of brain protection by erythropoietin(EPO) in epileptic brain damage of rats induced by lithium-pilocarpine.Methods Ninety-six SD rats aged 21-30 d were randomly divided into control group(n=32),lithium-pilocarpine epilepsy group(n=32) and EPO treated group(n=32),each group were subdivided into 4 groups(n=8) at 6 h,24 h,48 h and 72 h.Immunohistochemistry was used to analyze the expressions of CHOP and Caspase-12 in hippocampus areas of rats,and their behavior changes were observed.Results The expression of CHOP in hippocampus in epilepsy group increased gra-dually,6 h began to increase,reached peak at 24 h,then reduced gradually,but the expression of CHOP in 72 h was still higher than that in control group,there were signifiant difference of CHOP between the both groups at the same time points(Pa0.05).The expression of Caspase-12 in hippocampus in epilepsy group increased gradually,6 h began to increase,and then gradually increased,reached peak at 48 h,72 h began to decline,but the expressions were still higher than those in control group at the same time points(Pa0.05).In the EPO treated group,the level of CHOP and Caspase-12 in hippocampus at different time points had significant differences compared with those in epilepsy groups(Pa0.05).Conclusions The expressions of CHOP and Caspase-12 increases dramatically after epileptic discharges,which indicates that the mechanism of the endoplasmic reticulum stress could contribute to the occurrence and development of epileptic brain damage.EPO may produce brain protection by the mechanism of the endoplasmic reticulum stress.
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