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.