Expressions of glucose-regulated protein 78 and p38 mitogen-activated protein kinase signal pathway in the hippocampus of status convulsion rat and the effect of Nimodipine / 中华实用儿科临床杂志

ABSTRACT

Objective To explore the role of glucose-regulated protein 78 (GRP78),p38 mitogen-activated protein kinase(p38MAPK) signal pathway in seizure-reduced brain injures and the regulatory effect of Nimodipine on it.Methods Sprague-Dawley(SD) rats were randomly divided into status convulsion group (SC group),Nimodipine group(NM group),and a normal control group(NC group).The expressions of GRP78/Bip and p38MAPK mRNA and protein were detected by reverse transcription(RT)-PCR and immunohistochemistry.The expression of apoptosis cells was observed by TdT-mediated dUTP nick end labeling (TUNEL).Results (1) Immunohistochemistryat 4 h after induction of status convulsion,the expression of GRP78 protein in the hippocampus CA1 domain began increasing slightly,and reached a maximum at 24 h,and then began decreasing slowly ; at 4 h after induction of status convulsion,the expression of p38MAPK protein in the hippocampus CA1 domain began increasing,and reached a maximum at 24 h,and decreased remarkably at 48 h.(2) RT-PCRat 4 h after induction of status convulsion,the expression of GRP78 protein in the hippocampus CA1 domain began increasing slightly,and reached a maximum at 24 h,and then began decreasing slowly.The NM group was much higher than the SC group and the NC group(all P ＜ 0.05) ; at 4 h after induction of status convulsion,the expression of p38MAPK protein in the hippocampus CA1 domain began increasing,and reached a maximum at 24 h,and decreased remarkably at 48 h;the NM group was much lower than the SC group,and higher than the NC group (all P ＜ 0.05).(3) TUNELat 4 h after induction of status convulsion,the expression of the TUNEL positive cells in the hippocampus CA1 domain began increasing slightly,and reached a maximum at 48 h,and then began decreasing,and there was no difference between SC group and NC group;the NM group was much lower than the SC group(all P ＜ 0.05).Conclusions The correlation of the increased expression of p38MAPK and neuronal apoptosis indicates that GRP78 signal pathway may be mediated to cell apoptosis through p38MAPK.Nimodipine can affect the expression of GRP78/Bip and p38MAPK,and relieve endoplasmic reticulum stress,and lessen the pathologic damage to the hippocampus.