Effect of ischemic postconditioning on endoplasmic reticulum stress during cerebral ischemia/reperfusion in rats

Abstract

Objective To evaluate the ischemic postconditioning on endoplasmic reticulum stress during cerebral ischemia/reperfusion (I/R) in rats.Methods Ninety adult male Sprague-Dawley rats,aged 350-450 g,were randomly divided into 3 groups (n =30 each) using a random number table:sham operation group (S group),I/R group,and ischemic postconditioning group (group P).Focal cerebral I/R was induced by electrocoagulation of left middle cerebral artery and 30 min occlusion of bilateral common carotid arteries followed by reperfusion.In group P,bilateral common carotid arteries were subjected to 3 cycles of 30 s reperfusion and 10 s ischemia at the beginning of reperfusion.At 24 h of reperfusion,neurological deficit was scored,and cerebral infarct size was detected by TTC staining.At 6,12 and 24 h of reperfusion,the expression of glucose-regulated protein 78 (GRP78),C/EBP homologous protein (CHOP) and caspase-12 in the ischemic area were measured (using immunohistochemistry).The neuronal apoptosis in the ischemic area was detected by TUNEL.Results Compared with S group,the neurological deficit score was significantly increased,cerebral infarct size was enlarged,the neuronal apoptosis was increased,and the expression of GRP78,CHOP and caspase-12 was up-regulated in I/R and P groups.The neurological deficit score was significantly lower,cerebral infarct size was smaller,the expression of GRP78 was higher at 12 and 24 h of reperfusion,the neuronal apoptosis was lower at 24 h of reperfusion,and the expression of CHOP and caspase-12 was lower in group P than in group I/R.Concluion Ischemic postconditioning can inhibit neuronal apoptosis mediated by endoplasmic reticulum stress during cerebral I/R,which dose not play a leading role in cerebral protection in rats. Key words: Brain; Rreperfusion injury; Endoplasmic reticulum; Stress; Ischemic postconditioning