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The Effect Of Exercise Preconditioning On Apoptosis And Expression Of P53 And Bcl-2 In The Ischemic Penumbra Of Rats With Cerebral Ischemia Reperfusion

Posted on:2017-04-05Degree:MasterType:Thesis
Country:ChinaCandidate:X J WuFull Text:PDF
GTID:2284330482483632Subject:Rehabilitation Medicine & Physical Therapy
Abstract/Summary:PDF Full Text Request
Objective:The effect of exercise preconditioning on apoptosis and expression of p53 and Bcl-2 in the ischemic penumbra of rats with cerebral ischemia reperfusion. The aim was to clarify the mechanism of cerebral ischemic tolerance induced by exercise preconditioning, and to provide theoretical support for the prevention and treatment of ischemic stroke.Methods:The 36 male SD rats were randomly divided into 3 groups, namely, sham group, model group and exercise preconditioning group. Preparation of cerebral ischemia/reperfusion model of middle cerebral artery occlusion in rats by modified Longa suture method (MCAO). After I/R 2h,24h, through neural behavior scores of motor function were observed; After I/R 24h, rats in ischemic cortex pathological changes were examined by HE staining; TUNEL staining in the ischemic region was detected apoptosis in cortical neurons; Western blot was used to detect the ischemic area cortex p53 gene and bcl-2 protein expression.Result:1.The nerve function defect score:After I/R 2h,24h, sham group did not show nerve function injury. Model group of nerve function defect score in the above two time points were significantly higher than those in the sham group, the difference has statistical significance (P<0.01). After I/R 2h, exercise preconditioning group and model group of nerve function defect score differences had no statistical significance (P>0.05); After I/R 24h exercise preconditioning group of neural function defect score and model group compared to occur significantly decreased, the difference is statistically significant (P<0.01).2.Histopathology observation:After I/R 24h,, brain tissue of the sham group had no change, distinct cortical structure, structure and morphology of neural cells showed normal; model rats brain tissue ischemic cortex edema, cerebral ischemia loose organization and vacuolar change more obvious and characteristics of brain tissue ischemic central nerve cells showed necrosis, damage semi dark bands appeared apoptotic bodies. Compared with model group, exercise preconditioning rats brain tissue pathological changes showed different degrees of ease, regional brain injury was significantly lower than that in the model group decreased, the degeneration and necrosis of the cells significantly reduced the number, reduce the cell shrinkage abnormal phenomenon, apoptotic bodies is also reduced.3.The degree of apoptosis in ischemie penumbra:After I/R 24h, model rats cerebral ischemia penumbra of TUNEL positive cell number compared with the sham group high, exercise preconditioning group of TUNEL positive cell number compared with model group decreased significantly, the difference is statistically significant (P<0.05).4.The expression of p53-. Bcl-2 in ischemie penumbra:Sham operation group rats cerebral cortex p53 protein and bcl-2 protein were expressed, cerebral I/R 24h after ischemia model group, semi dark region of p53 protein and bcl-2 protein expression compared with the sham operation group increased significantly (P<0.01); pre treatment group ischemia penumbra region of p53 protein expression was significantly lower than that of model group, bcl-2 protein expression was much lower than that of model group increased significantly (P<0.01).Conclusion:1.Exercise preconditioning can reduce the neurological function score of cerebral I/R rats, reduce the pathological injury in the ischemic cortex area, and play a protective role in the brain.2.The expression of 2 down-regulated p53 in penumbra, the up-regulated expression of Bcl-2 Cerebral I/R injury can be reduced effectively by reducing the apoptosis of cortical cells in the cerebral ischemic area.
Keywords/Search Tags:Exercise Preconditioning, Cerebral Ischemia Reperfusion, Apoptosis, p53, Bcl-2
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