2011•Journal of Shandong UniversityRequires access

Activation of p38MAPK in pentylenetetrazol-induced seizure rats and intervention effect of pregabalin

Qiushi Li

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Abstract

Objective To explore activation of the p38MAPK signal pathway in pentylenetetrazol(PTZ)-induced seizure rats,and explore the intervention effect and mechanism of pregabalin(PBG),an inhibitor for γ-aminobutyric acid(GABA) receptors.Methods 38 adult Sprague-Dawley rats were randomly divided into 5 groups: the control group,the PTZ group and three doses of PBG-pretreated groups.After treatment with corresponding reagents,behavior,electrocorticogram and neuronal ultrastructural changes in the hippocampus were observed.Expression of p38MAPK in the hippoacampus of rats was determined by means of immunohistochemistry.Results Grade Ⅳ-Ⅴ of seizure was detected in the PTZ group,while grade Ⅰ-Ⅲ of seizure in PBG-pretreated groups(P0.05).Compared with the control group,expression of p38MAPK was increased in the PTZ group(P0.01),while it was decreased in PBG-pretreated groups compared with the PTZ group(P0.05).Among PBG-pretreated groups,grade of seizure and expression of p38MAPK were lower in high and medium dose groups compared with the low dose group.Conclusions Expression of p38MAPK is significantly increased in the hippocampus of PTZ-induced seizure rats.PBG has a protective effect on PTZ-induced seizure rats by depressing expression of p38MAPK.

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Objective To explore activation of the p38MAPK signal pathway in pentylenetetrazol(PTZ)-induced seizure rats,and explore the intervention effect and mechanism of pregabalin(PBG),an inhibitor for γ-aminobutyric acid(GABA) receptors.Methods 38 adult Sprague-Dawley rats were randomly divided into 5 groups: the control group,the PTZ group and three doses of PBG-pretreated groups.After treatment with corresponding reagents,behavior,electrocorticogram and neuronal ultrastructural changes in the hippocampus were observed.Expression of p38MAPK in the hippoacampus of rats was determined by means of immunohistochemistry.Results Grade Ⅳ-Ⅴ of seizure was detected in the PTZ group,while grade Ⅰ-Ⅲ of seizure in PBG-pretreated groups(P0.05).Compared with the control group,expression of p38MAPK was increased in the PTZ group(P0.01),while it was decreased in PBG-pretreated groups compared with the PTZ group(P0.05).Among PBG-pretreated groups,grade of seizure and expression of p38MAPK were lower in high and medium dose groups compared with the low dose group.Conclusions Expression of p38MAPK is significantly increased in the hippocampus of PTZ-induced seizure rats.PBG has a protective effect on PTZ-induced seizure rats by depressing expression of p38MAPK.

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Available abstract

Objective To explore activation of the p38MAPK signal pathway in pentylenetetrazol(PTZ)-induced seizure rats,and explore the intervention effect and mechanism of pregabalin(PBG),an inhibitor for γ-aminobutyric acid(GABA) receptors.Methods 38 adult Sprague-Dawley rats were randomly divided into 5 groups: the control group,the PTZ group and three doses of PBG-pretreated groups.After treatment with corresponding reagents,behavior,electrocorticogram and neuronal ultrastructural changes in the hippocampus were observed.Expression of p38MAPK in the hippoacampus of rats was determined by means of immunohistochemistry.Results Grade Ⅳ-Ⅴ of seizure was detected in the PTZ group,while grade Ⅰ-Ⅲ of seizure in PBG-pretreated groups(P0.05).Compared with the control group,expression of p38MAPK was increased in the PTZ group(P0.01),while it was decreased in PBG-pretreated groups compared with the PTZ group(P0.05).Among PBG-pretreated groups,grade of seizure and expression of p38MAPK were lower in high and medium dose groups compared with the low dose group.Conclusions Expression of p38MAPK is significantly increased in the hippocampus of PTZ-induced seizure rats.PBG has a protective effect on PTZ-induced seizure rats by depressing expression of p38MAPK.

Key concepts: Pentylenetetrazol, Immunohistochemistry, Hippocampus, Epilepsy, Pharmacology, Kainic acid, Medicine, Chemistry

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