Effects Of Ischemic Postconditioning On Endoplasmic Reticulum Stress Related Moleculars In Cerebral Ischemic/Reperfusion Injury

Objective: To study the protective effect of ischemic postconditioning onfocal cerebral ischemic/reperfusion injury in rats and to discuss the relationshipwith endoplasmic reticulum stress related moleculars GRP78and caspase-12.Methods: Adult male Wistar rats were randomly divided into threegroups for the experiment: sham group，ischemic/reperfusion（I/R）group andischemic postconditioning(IP) group. The latter two groups was respectivelyfuther divided into three subgroups:6h,12h and24h. Focal cerebralischemia/reperfusion model were induced by suture-occluded method toestablish middle cerebral artery occlusion. Then, the neurobehavioral scores,cerebral infarction volume and histopathology of cerebral ischemia wereassessed at24h of reperfusion. The expression of GRP78and caspase-12proteins in the ischemic penumbra were detected by immunohistochemistry andWestern blot from6h to24h of reperfusion.Results:①Compared with I/R group, ischemic postconditioningsignificantly reduced the neurobehavioral scores and cerebral infarction volume（P＜0.05）. HE stain: Compared with I/R group, the changes of histopathologyof cerebral ischemia were significant lighter in IP group.②Immunohistochemistry and Western blot： The expression of GRP78andcaspase-12proteins in I/R group were obviously higher than sham group from 6h to24h of reperfusion, and GRP78reached peak at12h, caspase-12reachedpeak at24h. In comparison to I/R group, the expression of GRP78protein weresignificantly increased in IP group from12h to24h of reperfusion（P＜0.05）,and the expression of caspase-12significantly reduced in IP group at24h ofreperfusion（P＜0.05）.Conclusions:①Cerebral ischemia/reperfusion causes endoplasmicreticulum stress.②Ischemic postconditioning improved neurological functionsand reduced cerebral infarction volume and pathology damage. Ischemicpostconditioning could protect brain against ischemia/reperfusion injury.③Ischemic postconditioning increased the expression of GRP78, whileinhibited the expression of caspase-12. The protection mechanism of theischemic postconditioning on cerebral ischemia/reperfusion injury may beattenuate endoplasmic reticulum stress.