Protection of edaravone on neurons and its effects on the expression of interleukin-lbeta in juvenile rat hippocampus following status convulsion.
- Author:
Hai-Ping WANG
1
;
Guang-Qian LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antipyrine; analogs & derivatives; pharmacology; Hippocampus; chemistry; drug effects; pathology; ultrastructure; Immunohistochemistry; In Situ Nick-End Labeling; Interleukin-1beta; analysis; Male; Neurons; drug effects; Neuroprotective Agents; pharmacology; Rats; Rats, Sprague-Dawley; Status Epilepticus; drug therapy; metabolism; pathology
- From: Chinese Journal of Contemporary Pediatrics 2010;12(3):205-210
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the possible protection of edaravone on neurons of the hippocampus after status convulsion (SC) and its effects on the expression of interleukin-1beta (IL-lbeta) in juvenile rats.
METHODSOne hundred and ninety-five juvenile male Sprague-Dawley rats were randomly divided into three groups: SC, edaravone pretreatment and normal saline control (control group). Each group was subdivided into five groups sacrificed at 4, 12, 24, 48 and 72 hrs after SC induction. SC model was prepared using lithium-pilocarpine. The edaravone pretreatment group received edaravone by intraperitoneal injection once daily three days before convulsion induction. Histopathologic changes in the hippocampus were viewed under a light microscope and an electron microscope. Expression of apoptosis cells was observed by TdT-mediated dUTP nick end labeling (TUNEL). Expression of IL-lbeta protein was determined by immunohistochemistry.
RESULTSUnder the electron microscrope, a small quantity of neurons showed karyopycnosis and endocytoplasmic reticulum (ER) expanded remarkably 24 hrs after SC induction; at 48 hrs the ER expanding was alleviated somewhat but mitochomdria swelling was more severe. The edaravone pretreatment group showed less severe neuronal changes compared with the SC group under the microscopes. The TUNEL positive cells in the hippocampus of the SC group were significantly more than those of the control group 12 hrs, and peaked at 48 hrs after SC induction. The edaravone pretreatment group showed decreased TUNEL positive cells in the hippocampus compared with the SC group, although the positive cells were more than those in the control group between 12 and 48 hrs after SC induction. The immunohistochemistry assay demonstrated that the expression of IL-lbeta in the hippocampus of the SC group increased significantly compared with that of the control group 12, 24, 48 and 72 hrs after SC induction. Edaravone pretreatment resulted in a significantly decreased IL-lbeta expression in the hippocampus as compared with the SC group.
CONCLUSIONSEdaravone pretreatment may decrease the IL-1beta expression and neuronal apoptosis in the hippocampus. This suggests that edaravone may have protective effects against the hippocampal damage caused by SC.