Neuronal Injury And Expression Of GRP78 And CHOP After Chronic Cerebral Ischemia

Objective:To observe the neurological function score and the expression of GRP78 and CHOP in hippocampus and cortex after chronic cerebral ischemic injury,and to give high mobility group protein B1(HMGB1)inhibitor to investigate the endoplasmic reticulum after chronic cerebral ischemia.The mechanism of apoptosis induced by neuronal apoptosis.Methods:Forty-eight adult healthy SD male rats were randomly divided into four groups: sham operation group(Sham),middle cerebral artery occlusion ischemia model group(MCAO),ethyl pyruvate(EP group)low dose group and high dose.The neurological function scores were observed by Longa5 method 5 weeks after model establishment.The behavioral differences of rats in each group were observed.The expressions of GRP78 and CHOP in hippocampus and cortex endoplasmic reticulum were detected by immunohistochemistry.Results:1.Neurological function scoreThere were no symptoms of neurological damage in the Sham group;the neurological deficit scores in the model group were higher,and the neurological scores in the EP group were negatively correlated with the EP dose,and were lower than the model group(P<0.05).2.Immunohistochemical staining results(1)GRP78 protein expression: no significant expression was found in hippocampus and cortex of Sham group;GRP78 protein was less expressed in model group(P<0.05);GRP78 expression in EP group was positively correlated with EP dose,and both were Higher than Model group(P<0.05).(2)CHOP protein expression: no apparent positive expression in hippocampus and cortex of Sham group;CHOP protein expression in model group was more negative;EP dose of EP in EP group was negatively correlated,and significant lower than model group(P<0.05).Conclusion:1.It is speculated that down-regulation of GRP78 expression and up-regulation of CHOP may enhance endoplasmic reticulum stress in chronic cerebral ischemic injury to aggravate neuronal damage.2.HMGB1 inhibitor pyruvate ethyl ester can reduce the endoplasmic reticulum stress after chronic cerebral ischemic injury by up-regulating GRP78 and down-regulating CHOP expression.