Edaravone protects against cerebral ischemia-reperfusion injury in rats by upregulation of the LMO4 expression
10.3760/cma.j.issn.1673-4165.2017.06.007
- VernacularTitle:依达拉奉通过上调LMO4表达保护大鼠脑缺血再灌注损伤
- Author:
Xianping XU
;
Chun HUANG
;
Fei YI
- Keywords:
Brain Ischemia;
Reperfusion Injury;
Antipyrine;
Free Radical Scavengers;
Neuroprotective Agents;
LIM Domain Proteins;
Disease Models;
Animal;
Rats
- From:
International Journal of Cerebrovascular Diseases
2017;25(6):526-530
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the neuroprotective mechanism of edaravone for cerebral ischemia-reperfusion injury in rats.MethodsThirty-six healthy adult male SD rats were randomly divided into three groups: a sham operation group, an ischemic model group, and an edaravone group (n=12 in each group).A focal cerebral ischemia model was induced by the suture method.Reperfusion was resumed after 2 h of ischemia;then the animals were sacrificed at 24 h after reperfusion.Edaravone 3 mg/kg was injected intraperitoneally immediately after cerebral ischemia-reperfusion in the edaravone group.The rats in the model group were injected equal volume normal saline.HE staining was used to observe the pathological changes.TUNEL staining was used to detect apoptotic cells in the ischemic cortex.Western blot and immunofluorescent staining were used to detect the expression levels of LIM domain protein 4 (LMO4) and LMO4 positive cells.Results HE staining showed that cellular morphology was basically normal in the sham operation group;both the model group and edaravone group had cell necrosis, but the latter was less severe.The number of morphologically normal cells in the edaravone group was significantly more than that in the model group (P<0.01).TUNEL staining showed that no TUNEL positive cells in the sham operation group were observed.The TUNEL positive cells in the edaravone group was significantly less that in the model group (P<0.01).Immunofluorescence staining showed that the expression level of LMO4 in the ischemic cortex in the edaravone group was significantly higher than that in the model group (P<0.01).ConclusionsEdaravone can alleviate the cerebral ischemia-reperfusion injury and inhibit neuronal apoptosis.Its mechanism may be associated with the upregulation of LMO4 expression.
