2009•Journal of Wenzhou Medical CollegeRequires access

Expression of JNK in the hippocampus of status convulsion rat and the effect of edaravone on it

Li We

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Abstract

Objective: To observe the change of JNK in the hippocampus of status convulsive rat and the regulation effect of EDA on it. Methods: One hundred and twenty male Juvenile Sprague-Dawley (SD)rats were randomly divided into normal control group(NC), status convulsivus group(SC), andedaravone group(EDA);and every group were randomly divided into five groups, which would be executed at 4 h,12 h,24 h,48 h and 72 h after convulsion discontinued. Status convulsivus(SC)was induced by injecting Lithium Chloride and Pilocarpine. Group EDA were injected EDA before convulsion,and repeatedly every day for 3 days. The expression of apoptosis cells were observed with TdT-mediated dUTP nick end labeling(TUNEL),the changes of p-JNK protein in the hippocampus CA1 domains were detected with immunohistochemistr(yIHC),the expression of JNK1 mRNA were detected with RT-PCR. Results: The TUNEL positive cells in hippocampus CA1 of SC group were more than that of NC group at 12 h after the S(CP 0.01). After the intervention of edaravone,TUNEL positive cells showed a significant drop( P 0.01 or P 0.05). The expression of p-JNK protein in the hippocampus CA1 domains increased markedly in SC group. The difference was statisticaly significance compared with NC group(P0.01), and EDA group was much lower than SC group(P0.01). The expression of JNK1 mRNA in the hippocampus in SC Group was much higher than NC Group (P 0.01),and EDA group was significantly lower than SC group(P 0.01). Conclusion: SC maybe increase the expression of JNK,JNK may be mediated to cell apoptosis. EDA can effect the expression of JNK, and lessen the pothology of hippocampus.

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Objective: To observe the change of JNK in the hippocampus of status convulsive rat and the regulation effect of EDA on it. Methods: One hundred and twenty male Juvenile Sprague-Dawley (SD)rats were randomly divided into normal control group(NC), status convulsivus group(SC), andedaravone group(EDA);and every group were randomly divided into five groups, which would be executed at 4 h,12 h,24 h,48 h and 72 h after convulsion discontinued. Status convulsivus(SC)was induced by injecting Lithium Chloride and Pilocarpine. Group EDA were injected EDA before convulsion,and repeatedly every day for 3 days. The expression of apoptosis cells were observed with TdT-mediated dUTP nick end labeling(TUNEL),the changes of p-JNK protein in the hippocampus CA1 domains were detected with immunohistochemistr(yIHC),the expression of JNK1 mRNA were detected with RT-PCR. Results: The TUNEL positive cells in hippocampus CA1 of SC group were more than that of NC group at 12 h after the S(CP 0.01). After the intervention of edaravone,TUNEL positive cells showed a significant drop( P 0.01 or P 0.05). The expression of p-JNK protein in the hippocampus CA1 domains increased markedly in SC group. The difference was statisticaly significance compared with NC group(P0.01), and EDA group was much lower than SC group(P0.01). The expression of JNK1 mRNA in the hippocampus in SC Group was much higher than NC Group (P 0.01),and EDA group was significantly lower than SC group(P 0.01). Conclusion: SC maybe increase the expression of JNK,JNK may be mediated to cell apoptosis. EDA can effect the expression of JNK, and lessen the pothology of hippocampus.

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Available abstract

Objective: To observe the change of JNK in the hippocampus of status convulsive rat and the regulation effect of EDA on it. Methods: One hundred and twenty male Juvenile Sprague-Dawley (SD)rats were randomly divided into normal control group(NC), status convulsivus group(SC), andedaravone group(EDA);and every group were randomly divided into five groups, which would be executed at 4 h,12 h,24 h,48 h and 72 h after convulsion discontinued. Status convulsivus(SC)was induced by injecting Lithium Chloride and Pilocarpine. Group EDA were injected EDA before convulsion,and repeatedly every day for 3 days. The expression of apoptosis cells were observed with TdT-mediated dUTP nick end labeling(TUNEL),the changes of p-JNK protein in the hippocampus CA1 domains were detected with immunohistochemistr(yIHC),the expression of JNK1 mRNA were detected with RT-PCR. Results: The TUNEL positive cells in hippocampus CA1 of SC group were more than that of NC group at 12 h after the S(CP 0.01). After the intervention of edaravone,TUNEL positive cells showed a significant drop( P 0.01 or P 0.05). The expression of p-JNK protein in the hippocampus CA1 domains increased markedly in SC group. The difference was statisticaly significance compared with NC group(P0.01), and EDA group was much lower than SC group(P0.01). The expression of JNK1 mRNA in the hippocampus in SC Group was much higher than NC Group (P 0.01),and EDA group was significantly lower than SC group(P 0.01). Conclusion: SC maybe increase the expression of JNK,JNK may be mediated to cell apoptosis. EDA can effect the expression of JNK, and lessen the pothology of hippocampus.

Key concepts: Hippocampus, TUNEL assay, Apoptosis, Convulsion, Internal medicine, Endocrinology, Chemistry, Medicine

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