Effect of butylphthalide and sodium chloride injection postconditioning on focal cerebral ischemia-reperfusion injury and endoplasmic reticulum stress in rats
10.3760/cma.j.issn.0254-1416.2013.12.019
- VernacularTitle:丁苯酞氯化钠注射液后处理对大鼠局灶性脑缺血再灌注损伤及内质网应激的影响
- Author:
Xiujing HUANG
;
Chunlin GAO
;
Guoyi Lü
- Publication Type:Journal Article
- Keywords:
Benzofurans;
Reperfusion injury;
Brain;
Endoplasmic reticulum;
Stress;
Ischemic postconditioning
- From:
Chinese Journal of Anesthesiology
2013;33(12):1485-1488
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of butylphthalide and sodium chloride injection postconditioning on focal cerebral ischemia-reperfusion (I/R) injury and endoplasmic reticulum stress in rats.Methods Thirty-six male SPF Sprague-Dawley rats,aged 2-3 months,weighing 260-280 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),focal cerebral I/R group (group I/R) and butylphthalide and sodium chloride injection postconditioning group (group Buty).The animals were anesthetized with intraperitoneal 10 ％ chloral hydrate 300 mg/kg.Focal cerebral I/R was induced by occluding right middle cerebral artery for 2 h followed by 24 h reperfusion in I/R and Buty groups.Butylphthalide and sodium chloride injection 2.5 mg/kg was injected via the tail vein immediately after onset of reperfusion in Buty group,while the equal volume of normal saline was injected in I/R group.Neurological deficits were assessed and scored at 24 h of reperfusion,and then the brain was isolated for detection of neuronal apoptosis (by TUNEL) and the expression of glucose-regulated protein 78 (GRP78) and caspase-12 in ischemic cerebral cortex (by immunohistochemistry) in brain tissues.Apoptosis index was calculated.Results Compared with group S,the neurological deficit scores and apoptosis index were significantly increased,and the expression of GRP78 and caspase-12 was up-regulated in I/R and Buty groups (P ＜ 0.05 or 0.01).Compared with group I/R,the neurological deficit scores and apoptosis index were significantly decreased,the expression of GRP78 was up-regulated,and the expression of caspase-12 was down-regulated in group Buty (P ＜ 0.05).Conclusion Butylphthalide and sodium chloride injection postconditioning can reduce focal cerebral I/R injury in rats,and inhibition of endoplasmic reticulum stressmediated cell apoptosis is involved in the mechanism.
