Mild hypothermia protects cerebral ischemia-reperfusion injury in rats by downregulating inhibitor of differentiation 2
10.3760/cma.j.issn.1673-4165.2017.03.006
- VernacularTitle:亚低温通过下调分化抑制因子2保护脑缺血再灌注损伤大鼠
- Author:
Li REN
;
Jin XING
;
Zilong WEI
;
Zhihan WANG
;
Liang ZHAO
;
Yongming QIU
;
Yingying LIN
- Keywords:
Brain Ischemia;
Reperfusion Injury;
Hypothermia;
Induced;
Inhibitor of Differentiation Protein 2;
Apoptosis;
Disease Models;
Animal;
Rats
- From:
International Journal of Cerebrovascular Diseases
2017;25(3):223-227
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of mild hypothermia on cerebral ischemia-reperfusion injury in rats and the effect of mild hypothermia on the expression of inhibitor of differentiation 2 (Id2) protein.Methods A total of 72 adult male rats were randomly divided into a sham operation group,a normothermia group,and a mild hypothermia group.A model of middle cerebral artery occlusion was induced by a suture method.The mild hypothermia group was treated with low temperature (anal temperature 33±1 ℃,tympanic membrane temperature 31±1 ℃).Modified Neurological Severity Score (mNSS) was used to evaluate neurological deficits,triphenyltetrazolium chloride staining was used to detect infarct volume,and Western blot was used to detect the Id2 expression in the ischemic cortex at ischemia-reperfusion 6,12,24,and 72 h,respectively.ResultsThe mNSS scores in the mild hypothermia group were significantly lower than those in the normothermia group,the infarct volumes were significantly smaller than those in the normothermia group at ischemia-reperfusion 6,12,24,and 72 h (all P<0.001).Western blot analysis showed that the Id2 expressions in the ischemic cortex in the mild hypothermia group were significantly lower than those in the normothermia group at ischemia-reperfusion 6,12,24,and 72 h (all P<0.05).Conclusion s Mild hypothermia can decrease neurological deficits and reduce infarct volume after cerebral ischemia-reperfusion,its mechanism may be associated with the down-regulation of the Id2 expression.
