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Objective:To study the effect of exercise preconditioning on the expression of autophagy-related protein Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3), and apoptosis after myocardial ischemia-reperfusion injury in rats, to explore the mechanism of myocardial protection by exercise preconditioning. Methods:A total of 36 male Sprague-Dawley rats were randomly divided into sham operation group, model group and exercise preconditioning group, with twelve rats in each group. The exercise preconditioning group received electric treadmill training for four weeks before modeling. The model of myocardial ischemia-reperfusion was made by ligation of the left anterior descending coronary artery 30 minutes and reperfusion. One hour after reperfusion, the expression of Beclin 1 and LC3 protein in myocardium was detected by Western blotting, and apoptosis of myocardial cells was observed by TUNEL staining, then the apoptotic index was calculated. Results:Compared with the model group, the level of LC3-I protein in the myocardial ischemic area increased, the levels of Beclin 1 and LC3-II decreased, the ratio of LC3-II/LC3-I decreased (P < 0.05); and the apoptotic index decreased in the preconditioning group (P < 0.05). Conclusion:Exercise preconditioning could up-regulate LC3-I in ischemic area, down-regulate the expression of Beclin 1 and LC3-II, and inhibit cardiomyocyte apoptosis after ischemia-reperfusion.
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BACKGROUND; At present, the mechanism of exercise preconditioning for myocardial protection has not been fully elucidated. It is reported that Rho/ROCK pathway plays a key role in cardiovascular disease. Whether exercise preconditioning adapts to the myocardium through the Rho/ROCK signaling pathway remains to be studied. OBJECTIVE: To investigate the role of exercise preconditioning in rats with myocardial injury after exhaustive exercise. METHODS: Sixty male Sprague-Dawley rats of 5 weeks old were randomly divided into three groups: Control group, simple exhaustive exercise group (EE group), and exercise preconditioning group after exhaustive exercise (EP+EE group). At 1 hour after modeling, a serum sample from each rat was taken for biochemical analysis. The levels of aspartate aminotransferase, phosphocreatine kinase, and lactate dehydrogenase were detected. Myocardial tissue samples from each rat were taken for pathological observation using hematoxylin-alkaline reddish-picric acid staining. TUNEL method was used to observe apoptosis in the myocardial tissue. The levels of tumor necrosis factor-a and interleukin-10 in the myocardial tissue were detected by ELISA. The expression of RhoA, ROCK1, ROCK2, Bax, and Bcl-2 protein was analyzed by western blot. RESULTS AND CONCLUSION: The levels of aspartate aminotransferase, phosphocreatine kinase, and lactate dehydrogenase of the EE group were significantly higher than those of the control group (P < 0.05). The levels of aspartate aminotransferase, phosphocreatine kinase, and lactate dehydrogenase of the EP+EE group were significantly lower than those of the EE group (P < 0.05). The boundary of cardiomyocytes was unclear in the EE group, in which there were more plaque-like or flaky red-like areas as well as more obvious ischemia-anoxia changes as compared with the control group. Some cardiomyocytes presented with unclear boundary in the EP+EE group with some plaque-like brilliant red-like areas, and the degree of ischemia and anoxemia was significantly lower in the EP+EE group than the EE group. The apoptotic index value of the EE group was significantly higher than that of the control group, and the apoptotic index value of the EP+EE group was significantly lower than that of the EE group (P< 0.05). The tumor necrosis factor-a and interleukin-10 levels in the EE group were significantly higher than those in the control group (P < 0.05). The tumor necrosis factor-a and interleukin-10 levels in the EP+EE group were significantly lower than those in the EE group (P < 0.05). The Bcl-2/Bax of the EE group was significantly lower than that of the control group (P < 0.05). The Bcl-2/Bax of the EP+EE group was significantly higher than that of the EE group (P < 0.05). The levels of RhoA, ROCK1 and ROCK2 in the EE group were significantly higher than those in the control group. The levels of RhoA, ROCK1 and ROCK2 in the EP+EE group were significantly lower than those in the EE group (P < 0.05). These findings indicate that exercise preconditioning has a protective effect against myocardial injury and improves cardiac function in rats. The mechanism may be related to the Rho/ROCK pathway.
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Objective:To observe the effects of exercise preconditioning on blood-brain barrier (BBB) permeability, and connexin 43 (Cx43) and pannexin 1 (Panx1) protein after cerebral ischemia-reperfusion injury in rats. Methods:Fifty-four male Sprague-Dawley rats were randomly divided into sham group (n = 18), model group (n = 18) and exercise preconditioning group (n = 18). The exercise preconditioning group was trained with treadmill for three weeks before modeling. The middle cerebral arteries were occluded in the model group and the exercise preconditioning group using the modified Koizumi suture. After reperfusion of 24 hours, the rats were assessed with modified Neurological Severity Score (mNSS). The permeability of BBB was observed with Evans blue (EB). The expression of Cx43 and Panx1 was detected with Western blotting and immunohistochemistry in the ischemic tissues. Results:Compared with the model group, the mNSS score decreased in the exercise preconditioning group (P < 0.05), while the Evans blue content and the expression of Cx43 and Panx1 decreased (P < 0.05), as well as the the positive areas of Cx43 and Panx1 (P < 0.05). Conclusion:Exercise preconditioning can improve the permeability of BBB in cerebral ischemia-reperfusion rats, which may associate with down-regulation of Cx43 and Panx1, to protect brain from injury.
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@#Objective To explore the effect and mechanism of exercise preconditioning on neurological deficits in rats after cerebral ischemia-reperfusion. Methods Thirty-six healthy Sprague-Dawley rats were randomly divided into sham group (n=12), model group (n=12) and exercise preconditioning group (n=12). The latter two groups were occluded middle cerebral artery for 120 minutes and reperfused with modified suture method. The rats were evaluated with Longa's score two, twelve and 24 hours after reperfusion. The expression of mitochondrial ATP-sensitive potassium (mitoKATP) channel proteins inwardly rectifying potassium channel (Kir6.2) and sulphonylurea receptor 1 (SUR1) were detected with Western blotting and the cerebral cell apoptosis was detected with TUENL assay 24 hours after reperfusion. Results Compared with the model group, the Longa's score decreased in the exercise preconditioning group 24 hours after reperfusion (P<0.05), while the expression of Kir6.2 and SUR1 decreased (P<0.05), and TUNEL-positive cells decreased (P<0.05).Conclusion Exercise preconditioning may improve neurological function after cerebral ischemia-reperfusion, which may associate with inhibiting the expression of mitoKATP channel proteins and cell apoptosis.
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Objective To observe the heart protective effect of exercise preconditioning (EP) in the acute exhaustion exercise (EE) rats, and explore its action mechanism further. Methods Eighty healthy male Sprague-Dawley (SD) rats were divided into control group (C group), EP group, EE group, and EP+EE group randomly, with 20 rats in each group. The rats in EP and EP+EE groups were trained for 3 weeks according to the daily swimming for 60 minutes (swimming 15 minutes, resting 5 minutes, repeating 3 times) with 6 days each week. The rats in EE and EP+EE groups on the last 1 day after 3 weeks, 3% weight heavy weight was carried once for swimming EE. Two hours after the last EE, abdominal aortic blood and heart was harvested, the levels of serum MB isoenzyme of creatine kinase (CK-MB) and calcitonin gene related peptide (CGRP) were determined by enzyme linked immunosorbent assay (ELISA); the ultrastructure of myocardium was observed by optical microscopy; the levels of myocardial malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by ELISA, the mRNA expression of myocardial CGRP was assayed by reverse transcription-polymerase chain reaction (RT-PCR), and the protein expression of myocardial CGRP was assayed by Western Blot. Results Compared with C group, the levels of serum CK-MB and myocardial MDA were significantly increased, serum CGRP content, myocardial SOD activity, and mRNA and protein expressions of myocardial CGRP were significantly decreased in EE group and EP+EE group. Compared with EE group, the levels of serum CK-MB and myocardial MDA in EP+EE group were decreased [CK-MB (U/L): 13.11±0.77 vs. 15.55±0.90, MDA (μmol/L): 389.57±49.60 vs. 709.08±160.49], the level of serum CGRP, and mRNA and protein expressions of myocardium CGRP were increased [serum CGRP (ng/L): 120.41±9.07 vs. 97.97±9.05, CGRP mRNA (2 -ΔΔCT): 0.45±0.09 vs. 0.14±0.02, CGRP protein (gray value): 0.78±0.08 vs. 0.41±0.04, all P < 0.05], the degree of myocardial injury was obviously alleviated. There was no significant difference in the indexes between the EP group and C group. Conclusion EP has the heart protective effect for the acute EE rats, and the mechanism is closely related to the endogenous protective substance CGRP.
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Objective To compare the expression of myocardial connexin 43(Cx43)mRNA and its protein during early and late cardioprotection stages of exercise preconditioning.Methods Thirty-two Sprague-Dawley rats were randomly divided into a control group,an exhaustive exercise(EE)group,an early exercise preconditioning + exhaustive exercise(EEP+EE)group and a late exercise preconditioning + exhaustive exercise (LEP+EE) group,each of 8.All groups were given intervention as their group name indicated.Then in situ hybridization and real-time fluorescent quantitative PCR methods were used to detect the changes of myocardial Cx43mRNA and immunohistochemical method and Western blotting were used to detect the changes of Cx43 protein.Results Compared with EE group,there was significant increase in Cx43 mRNA and its protein expression in group EEP+EE and LEP+EE.Compared with EEP+EE group,no significant changes was found in situ hybridization and Cx43 Immunoreactivity in LEP+EE group,neither did significant differences in the expression of Cx43 mRNA and its protein.Conclusion EEP and LEP can significantly promote the expression of myocardial Cx43 mRNA and its protein respectively.However there is no significant changes of myocardial Cx43 mRNA and protein expression between the 2 time phases.It demonstrates that the expression of Cx43 in the early and late stage of myocardial protective effect was consistent with the changes of the early and late phase of the protective effect of EP.
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Objective To discuss the mechanism about exercise preconditioning (EP) protected myocardium by means of regulate NLRP3 inflammasome signal pathways on exhausted exercise rats. Methods The male Sprague-Dawley (SD) rats were randomly divided into four groups: normal control group (C group), no EP on exhausted exercise group (EE group), 3dEP + EE group, and 3wEP + EE group, with 12 rats in each group. In C group and EE group, the rats had not done exercise, while EE group took an exhausted swimming exercise with 3% heavy weight on tail at the end of 3 weeks; 3dEP + EE group and 3wEP + EE group exercised according to the standard of swimming for 60 minutes every day (swam 15 minutes, took a rest for 5 minutes, repeated 3 times), 6 days in a week, and were trained for 3 days and 3 weeks respectively, and took an exhausted swimming exercise on the last day. A light microscope and electron microscope were used to observe the myocardial histopathology and ultrastructure change, and enzyme linked immunosorbent assay (ELISA) was used to detect the levels of serum interleukin (IL-1β, IL-18, IL-6), hypersensitive C-reactive protein (hs-CRP), MB isoenzyme of creatine kinase (CK-MB), and brain natriuretic peptide (BNP). The protein expressions of NLRP3 and caspase-1 were detected by Western Blot. The correlations among all the parameters were analyzed by Pearson correlation analysis. Results Under the light microscope and electron microscope, the myocardial fiber morphological structure was normal, neatly, and no interstitial edema, muscle membrane damage or myocardial cell swellen was found in C group. In EE group, heart tissues were stained obviously uneven, a large number of myocardial fibers were fractured and messed, interstitial fibers were hyperplasiaed and edema moderately, much of myocardial cells were edema and necrosis, inflammatory cells were infiltrated, the number of average infiltration inflammatory cells was highest, mitochondria were edema seriously, part of the crest and a small number of membrane were blended together, fuzzy and crest were fractured, sarcomere were disordered; 3dEP + EE group and 3wEP + EE group heart tissues injuries were obviously alleviated, among the three groups, and the best results were in 3wEP + EE group. Compared with C group, the serum contents of IL-1β, IL-18, IL-6, hs-CRP, CK-MB, BNP and heart tissues protein expressions of NLRP3 and caspase-1 in EE group were significantly increased [IL-1β (μg/L): 18.77±1.28 vs. 12.00±1.55, IL-18 (μg/L): 236.79±15.73 vs. 150.74±7.09, IL-6 (μg/L): 59.31±9.17 vs. 34.65±2.89, hs-CRP (mg/L): 469.37±137.73 vs. 107.15±14.22, CK-MB (U/L): 15.57±0.91 vs. 7.40±0.40, BNP (ng/L): 532.08±63.44 vs. 386.96±34.77, NLRP3 protein (gray value): 0.66±0.07 vs. 0.16±0.06, caspase-1 protein (gray value): 0.96±0.08 vs. 0.48±0.06, all P 0.05]. A positive correlation was shown among IL-1β, IL-18, IL-6, hs-CRP, BNP, CK-MB, NLRP3, and caspase-1 (all P < 0.01). Conclusions EP can reduce inflammatory reaction by regulating the NLRP3 inflammatory signal pathways, and protect the myocardial injury. The protection of the heart by long-term EP is more obvious than that of short-term EP.
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@#Objective To explore the effect of exercise preconditioning on apoptosis and expression of P53 protein in ischemic penum-bra in rats after cerebral ischemia-reperfusion. Methods Thirty-six Sprague-Dawley rats were randomly divided into sham group, model group and exercise preconditioning group, with twelve rats in each group. The middle cerebral artery occlusion (MCAO) model was estab-lished with modified Longa's method. TUNEL method was used to observe the apoptosis of neural cells in the ischemic penumbra. Western blotting was used to detect the expression of P53 protein in the ischemic penumbra. Results Twenty-four hours after cerebral ischemia-reper-fusion, the number of TUNEL positive cells was more in the model group than in the sham group (P<0.01), and was less in the exercise pre-conditioning group than in the model group (P<0.01). The expression of P53 protein was higher in the model group than in the sham group (P<0.01), and was lower in the exercise preconditioning group than in the model group (P<0.01). Conclusion Exercise preconditioning coud down-regulate the expression of P53 protein in the ischemic penumbra, and inhibit the apoptosis of cortical cells.
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Objective To investigate the effect of exercise preconditioning on the expression of nerve growth factor(NGF) and its receptor TrkA as well as learning-and-memory abilities in rats suffered from focal cerebral ischemia.Methods Thirty-six male SD rats were randomly divided into sham operation group (Sham-MCAO,n=12),focal cerebral ischemia-reperfusion group (MCAO,n=12) and exercise preconditioning + cerebral ischemia-reperfusion group (EX+MCAO,n=12).Rats in EX+MCAO group were placed in the treadmill device and accepted 4 weeks exercise training.Then method of middle cerebral artery occlusion was applied to prepare transient focal cerebral ischemia reperfusion model.Garcia's method was used to assess the neural function in rats.Western blotting was applied to test the expression of NGF and TrkA protein in the successfully established experimental MCAO rats.Morris water maze experiment was uti lized to test the learning-and-memory abilities of the rats.Results (1) Compared with Sham-MCAO group,the expression of NGF in rats' brain tissue was lower in MCAO group (cerebral ischemia 1h reperfusion 24h) (P＜0.05).The expression of NGF of EX+MCAO group was higher than that of MCAO group,but still lower than that of Sham-MCAO group (P＜0.05).(2)The expression of TrkA in rats' brain tissue was higher in MCAO group compared with Sham-MCAO group (P＜0.05).Compared with MCAO group,the expression of TrkA was even higher in EX+MCAO group (P＜0.05).(3)On the fifth day in the Morris water maze test,the latency of MCAO group was significantly longer than that of Sham-MCAO group((9.36± 1.18)s vs (4.86± 1.52) s,P＜0.05).However,compared with MCAO group,the latency in EX+MCAO group ((6.02± 1.04) s) was shorter,but still longer than Sham-MCAO group (P＜0.05).There was no significant difference among the three groups in the average swimming speed (P＞0.05).Conclusion Exercise preconditioning can up-regulate the expressions of NGF and TrkA protein,which can also improve the learning-and-memory abilities in rats suffered from focal cerebral ischemia reperfusion injury.
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Objective To investigate the effect of exercise preconditioning on serum level of tumor necrosis factorα(TNF-α), interleu-kin (IL)-1βand IL-6 in rats after cerebral ischemia-reperfusion (I/R). Methods 24 male Sprague-Dawley rats were randomly divided into exercise preconditioning group (n=8), model group (n=8) and sham group (n=8). The middle cerebral arteries were occluded for 120 min and re-perfused. All the rats were evaluated with neurological deficit score 2 hours, 24 hours after I/R. The serum levels of TNF-α, IL-1βand IL-6 was detected with enzyme-linked immunosorbent, and the pathology was observed with HE staining 24 hours after I/R. Results The neurological deficit score decreased in the exercise preconditioning group compared with that in the model group, as well as the serum TNF-α, IL-1βand IL-6 (P<0.05) 24 hours after I/R. The pathological damage and interstitial edema alleviated in cerebral ischemia cortical, and the degeneration and necrosis of the neurons in the ischemic area significantly reduced in the exercise preconditioning group. Conclu-sion Exercise preconditioning may inhibit inflammatory response in I/R rats to protect neurological function from impairment.
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Cerebral ischemia tolerance was induced by exercise preconditioning, which protected the brain from injury. The detailed mechanism of exercise preconditioning protecting cerebral ischemia injury was complicated, which involving the regulation of multiple tar-get point and multi-path, such as inhibiting cell apoptosis, promoting angiogenesis in the brain, inhibiting the excessive activation of glutam-ic acid as well as the regulation of inflammation. More mechanisms were still unknown.
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Objective:To investigate the expression of myocardium connexin 43 (Cx43) in late exercise preconditioning (LEP) cardioprotection.Methods: Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups (n=8). Myocardial injury was judged in accordance with serum levels of cTnⅠ and NT-proBNP as well as hematoxylin basicfuchsin picric acid staining of myocardium.Cx43mRNA was detected byin situhybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting.Results:The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43mRNA level between the four groups. Cx43 protein level was decreased significantly in group EE (P<0.05). However, LEP produced a significant increase in Cx43 protein level (P<0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP (P<0.05).Conclusions:LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43.
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Objective: To investigate the expression of myocardium connexin 43 (Cx43) in late exercise preconditioning (LEP) cardioprotection. Methods: Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups (n = 8). Myocardial injury was judged in accordance with serum levels of cTn[U+2160] and NT-proBNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 mRNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting. Results: The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 mRNA level between the four groups. Cx43 protein level was decreased significantly in group EE (P < 0.05). However, LEP produced a significant increase in Cx43 protein level (P < 0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP (P < 0.05). Conclusions: LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43.
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@#Objective To investigate the effect of exercise preconditioning on serum level of tumor necrosis factor α (TNF-α), interleukin (IL) -1β and IL-6 in rats after cerebral ischemia-reperfusion (I/R). Methods 24 male Sprague-Dawley rats were randomly divided into exercise preconditioning group (n=8), model group (n=8) and sham group (n=8). The middle cerebral arteries were occluded for 120 min and re-perfused. All the rats were evaluated with neurological deficit score 2 hours, 24 hours after I/R. The serum levels of TNF-α, IL-1β and IL-6 was detected with enzyme-linked immunosorbent, and the pathology was observed with HE staining 24 hours after I/R. Results The neurological deficit score decreased in the exercise preconditioning group compared with that in the model group, as well as the serum TNF-α, IL-1β and IL-6 (P<0.05) 24 hours after I/R. The pathological damage and interstitial edema alleviated in cerebral ischemia cortical, and the degeneration and necrosis of the neurons in the ischemic area significantly reduced in the exercise preconditioning group. Conclusion Exercise preconditioning may inhibit inflammatory response in I/R rats to protect neurological function from impairment.
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OBJECTIVE@#To investigate the expression of myocardium connexin 43 (Cx43) in late exercise preconditioning (LEP) cardioprotection.@*METHODS@#Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups (n = 8). Myocardial injury was judged in accordance with serum levels of cTnⅠ and NT-proBNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 mRNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting.@*RESULTS@#The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 mRNA level between the four groups. Cx43 protein level was decreased significantly in group EE (P < 0.05). However, LEP produced a significant increase in Cx43 protein level (P < 0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP (P < 0.05).@*CONCLUSIONS@#LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43.
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Objective: To explore the effect of exercise preconditioning (EP) on pathological cardiac hypertrophy and heart failure (HF) in pressure over-loaded experimental rats. Methods:A total of 60 SD rats at the age of 6 weeks were randomly divided into 3 groups, n=20 in each group. Sham-operation group, Transverse aortic constriction (TAC) group and EP + TAC group. The cardiac function and structure were evaluated by echocardiography, patholgical changes and HF biomarkers were examined for EP effect at 4 and 8 weeks after TAC. Results:Compared with Sham-operation group, the cardiac function and structure had obvious changes in the other 2 groups. Compared with TAC group, the ejection fraction in EP+ TAC group increased 15%, the heart weight index and left ventricular weight index decrease 15.7%and 20%respectively at 8 weeks after TAC, all P Conclusion: EP may improve cardiac pathological hypertrophy in pressure over-loaded rats at the early stage, and delay the heart failure process.
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Objective The goal of this study was to explore the effect of exercise preconditioning on the expression of calcitonin gene-related peptide(CGRP)in the dorsal root ganglion of rats.Methods Fifty healthy male SD rats were randomly divided into control group (C) and exercise preconditioning group(EP).Group EP performed intervial treadmill exercise for 3 weeks for establishing exercise preconditioning animal model.The expression of CGRP mRNA in dorsal root ganglion was investigated by real-time fluorescence quantitative PCR.The immunoreaetion of CGRP in dorsal root ganglion was shown by immunohistochemistry.Results There was no significant difference in the expression of CGRP mR.NA in two groups(P>0.05).As compared with the group C,the immunoreaction of CGRP was increased in group EP,and the positive area and mean optical density of CGRP immunoreaction in group PE were significant higher than that in group C(P<0.05).Conclusion Exercise preconditioning does not change the expression of CGRP mRNA in dorsal root ganglion,but enhances the expression of CGRP in dorsal root ganglion to promote the reserve and release of CGRP in peripheral nerve endings and has the same endogenous protection as ischemie preconditioning.
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AIM: To explore the delayed protection of heme oxygenase-1 (HO-1) in the exercise preconditioning (EP) from the myocardial relative ischemia reperfusion injury (rI/R). METHODS: 40 Wistar Rats were divided into 5 groups randomly: control group (CN), rI/R group (IR), EP+rI/R group (EI), HO-1 inductor hemin+rI/R group (HE) and HO-1 inhibitor ZnPP+EP+rI/R group (EZ). The following indexes were detected, including the HO-1activity in myocardium, the cardiac function parameter-pressure-rate product (heart rate × left ventricular developed pressure, PRP) and the content of MDA in coronary effluent. RESULTS: After myocardial rI/R, HO-1 activity increased significantly. Moreover, EP or HO-1 inductor could enhance this effect manifestly. Nevertheless, when the HO-1 inhibitor was administered before EP,HO-1 activity decreased. In addition, there was no distinct difference in the HO-1 activity between EI group and HE group. At the 30 min point of reperfusion, the PRP recovery rate of EI group was higher clearly than that of IR group. However, there was reverse effect between the EZ group and the EI group. The MDA in coronary effluent of EI group, EZ group and HE group were lower obviously than that of IR group and there was significant difference between EI group and EZ group. CONCLUSION: EP could protect the heart from the rI/R injury occurring 24 hours later, which might be performed through activating the HO-1.