Exercise Preconditioning Affects Endoplasmic Reticulum Stress-mediated Cell Apoptosis After Cerebral Ischemia-reperfusion Injury In Rats

Objective:A foeal cerebral ischemia rat model was used in The study.We explore the Protective effeet of exercise preconditioning against isehemia-repefusion injury.The aim is to investigated whether the protective mechanism is related to the apoptosis caused by endoplasmic reticulum stress.Methods:Eighty adult Sprague-Dawley rats were randomly divided into the four groups: the sham group(S),the simple exercise group(SE),the model group(M)and the exercise intervention group(EI).Four-week treadmill exercise was performed in the SE group and the EI group.The model was established by placement of a suture to block the middle carotid artery,and reperfusion was triggered by suture removal.The samples were taken at 24 hours after ischemia.The S group only separated the right common carotid artery,internal carotid artery and external carotid artery,and no plug was inserted.The middle cerebral artery occlusion-reperfusion injury model was established in the M group,and the middle cerebral artery occlusion-reperfusion injury model was established in the EI group after exercise.The neurological deficits of the rats were evaluated at rats after 24 hours of ischemia.The infarct volume of the rats was assessed by TTC method.The apoptosis of the penumbra was detected by Tunel method.grp78 and caspase-3 protein expression were evaluated by immunohistochemistry,grp78,caspase-3 and chop protein expression were evaluated by western blots.Results:Neurological deficits was normal in S group and SE group,Longa score was 0 points.The Longa score of M group and the EI group was significantly higher than in S group(P < 0.05),The Longa score of the EI group was significantly lower than in M group at 24 hours after reperfusion(P<0.05).All brain slices were stained red in S group and SE group with no cerebral infarction area.The infarct volume of the rats in EI group was significantly lower than that in the M group(P<0.05).TUNEL staining showed that only a small number of TUNEL positive cells were found in the penumbra of rats in S group and SI group.Apoptotic cells in M group and EI group increased significantly,which was higher than that in S group(P < 0.05),and thenumber of TUNEL positive cells in EI group was significantly lower than that in model group(P < 0.05).Compared with S group,the expression of caspase-3 in cerebral cortex of SE group increased slightly,but there was no statistical significance(P>0.05).Compared with S group,caspase-3 protein expression in M group increased significantly at 24 hours of reperfusion(P<0.05),Compared with M group,exercise preconditioning Significant inhibited the expression of caspase-3(P<0.05).Compared with S group,the expression of endoplasmic reticulum stress-related factor grp78 and chop in M group increased significantly at 24 hours of reperfusion(P<0.05).Exercise preconditioning significant inhibited the expression of grp78 and chop(P<0.05).Conclusions:1.Four-week exercise preconditioning can improve neurological deficit and reduce cerebral infarction volume after 24 hours of reperfusion in rats,and which has a protective effect on cerebral ischemia injury.2.Exercise preconditioning can reduce the apoptotic rate of ischemic penumbra after24 hours of reperfusion in rats,inhibit the expression of caspase-3 and reduce the occurrence of apoptosis.3.Exercise preconditioning can reduce the expression of endoplasmic reticulum stress-related markers grp78,chop after cerebral ischemia-reperfusion injury,inhibit the increase of endoplasmic reticulum stress level to alleviate cerebral ischemia-re perfusion injury.