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1.
AIM: To study the expression of Fas/FasL mRNA in lung tissue with ischemia-reperfusion lung injury in rabbits and the relationship with the apoptosis,and to observe the effects of Tertram ethylpyrazine on them.METHODS: The pulmonary ischemia-reperfusion models in rabbits with occlusion of left pulmonary hilum for 1 h and then reperfusion 1,3,5 h respectively were used in this experiment.In TMP group,Tertram ethylpyrazine was intravenously dropped at dose of 60 mg/kg at 1 h before ischemia.The TUNEL technique was used to explore apoptotsis of pulmonary cells.In situ hybridization was performed on the rabbit lung tissue to assay the expression of Fas/FasL mRNA.RESULTS: Apoptosis of pulmonary cells was found in both IR group and TMP group.Compared with group IR,the apoptosis index (AI) was decreased obviously in group TMP (P<0.01).There was a significant positive correlation between the expression of Fas/FasL mRNA and the apoptosis of pulmonary cells (r1=0.900,r2=0.869,P<0.01).CONCLUSION: The activation of Fas/Fas-L system may contribute significantly to induce pneumocyte apoptosis in pulmonary ischemic injury.Tertram ethylpyrazine inhibits the activation of Fas/FasL system to decrease apoptosis in pulmonary tissue,which may protect the pulmonary tissues in ischemia injury.  相似文献   

2.
AIM: To explore the relationship between apoptosis in the lung tissues and lung ischemia/reperfusion injury, and to observe the effects of human thioredoxin (hTrx) on apoptosis in lung ischemia/reperfusion injury. METHODS: The single lung in situ ischemia/reperfusion animal model was used. Eighty four Wistar rats were randomly divided into control group (control), groups of ischemia for 1 h and reperfusion for different times (IR1h, IR3h, IR5h), and groups of IR+human thioredoxin treatment (IR1h +hTrx, IR3h +hTrx and IR5h +hTrx). Transmission electron microscope (TEM), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunocytochemistry techniques were used to observe apoptosis, apoptosis signal-regulating kinase 1 (ASK1) and expression of Bcl-2 and Bax in various phases of lung ischemia/reperfusion. RESULTS: Cell apoptosis in lung tissues was significantly high, ASK1, Bcl-2 and Bax protein were up-regulated in lung tissues of lung ischemia/reperfusion injury as compared to control (all P<0.01). Compared to IR group, hTrx suppressed apoptosis as well as expression of ASK1 and Bax protein (P<0.01), Bcl-2 protein and the ratio of Bcl-2/Bax were up-regulated in lung tissues (all P<0.05 or P<0.01). There was a significant correlation between the expression of ASK1, Bax protein and cell apoptosis (r=0.775, r=0.814, respectively; all P<0.01). There was a negative correlation between cell apoptosis and Bcl-2/Bax protein (r=-0.275, P<0.05). CONCLUSION: Initiating cell apoptosis by the activation of Bcl-2/Bax system in lung tissues may contribute to the pathogenesis of lung ischemia/reperfusion injury. The protective effects of hTrx include suppressing the expression of ASK1, down-regulating the ratio of Bcl-2/Bax and blocking apoptosis in lung tissues in lung ischemia/ reperfusion injury.  相似文献   

3.
AIM：To investigate the effect of puerarin (Pur) on expression of Fas/FasL mRNA in lung tissue during pulmonary ischemia and reperfusion injury (PIRI) in rabbits.METHODS：Single lung ischemia and reperfusion animal model was used.The rabbits were randomly divided into three groups,sham operated group (sham,n=10),PIR group (I-R,n=30) and PIR+ Pur group (Pur,n=30).Changes of several parameters included apoptotic index (AI),wet to dry ratio of lung tissue weight (W/D) and index of quantitative assessment of histologic lung injury (IQA) were measured at 60,180 and 300 minutes after reperfusion in lung tissue.Meanwhile,the location and expression of Fas/FasL mRNA were observed.Lung tissue was prepared for light microscopic and electron microscopic observation at 60,180,300 minutes after reperfusion.RESULTS：As compared with group I-R,Fas/FasL mRNA slightly expressed in intima and extima of small pulmonary artery,alveoli,and bronchiole epithelia in group Pur.The values of AI,W/D and IQA showed significantly lower than that in group I-R at 60,180,300 minutes after reperfusion in lung tissue (P<0.01 and P<0.05).Meanwhile,abnormal changes of the lung tissue in morphologically were lessen markedly in group Pur.CONCLUSION：Puerarin produces a notable protective effects on PIRI in rabbits by inhibiting Fas/FasL mRNA expression and decreasing apoptosis.  相似文献   

4.
AIM: To discuss the effect of Fas/FasL on the late reperfusion of acute myocardial infarction (AMI) and the potential oxidative stress mechanism. METHODS:Eighteen anesthetized dogs were randomly divided into three groups: late reperfusion group (n=6): ligated the coronary for 6 h, followed by reperfusion for 6 h; permanent ischemia group (n=6): after pericardium were opened for 6 h, ligated the coronary for 6 h, and did not reperfuse; control group (n=6): did not ligate the coronary but operation last for 12 h. Infarction brim myocardial Fas/FasL was detected by immunohistochemistry. Apoptosis index (AI) was detected by TUNEL. SOD and GR activity and MDA content were detected by colorimetry. RESULTS:The expression of Fas/FasL and apoptosis index were significantly higher in permanent ischemia group and late reperfusion group than those in control group (P<0.05, P<0.01), and the difference between them was also significant (P<0.05). SOD and GR activities were lower in permanent ischemia group and late reperfusion group than those in control group (P<0.05, P<0.01). The MDA contents in permanent ischemia group and late reperfusion group were higher than that in control group (P<0.05). CONCLUSION:The late reperfusion of AMI promotes the expression of Fas/FasL and myocardial apoptosis, and it may be due to oxidative stress mechanism.  相似文献   

5.
AIM: To observe the effect of leptin (LEP) on hypoxia-reoxygenation induced apoptosis in L02 cells.METHODS: In the experiment, L02 cell injury was induced by hypoxic air (95%N2 and 5% CO2). The cultured L02 cells were divided into hypoxic 12 h group (IR group) alone, normal control group and the hypoxic plus leptin (100 μg/L, 200μg/L, 400 μg/L, 800 μg/L and 1 600 μg/L) treatment groups in vitro. Flow cytometry, terminal dUTP nick-end labeling (TUNEL) assay and fluorescent quantitative PCR were used to measure the changes of apoptosis in L02 cells and expression of Fas/FasL mRNA.RESULTS: (1) The percentage of L02 cells apoptosis and positive TUNEL cells significantly increased in IR group compared to control group (P<0.01). When L02 cells were treated with LEP, the percentage of cell apoptosis and positive TUNEL cells were decreased compared to IR group. (2) Compared to control group, the Fas/FasL mRNA expression significantly increased in IR group (P<0.01). When L02 cells were treated with LEP, the Fas/FasL mRNA expression decreased compared to IR group, the effect of LEP at concentration of 400 μg/L was obviously (P<0.05). CONCLUSION: LEP decreases the apoptosis of hypoxic-reoxygenation L02 cells by down-regulation of Fas/FasL mRNA expression in L02 cells.  相似文献   

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7.
AIM: To investigate the effets of naoluo xintong on the expression of Fas, FasL protein in hippocampus CA1 area and Fas mRNA in the cortex of frontal or parietal lobe after local cerebral ischemia/reperfusion in MCAO rats. METHODS: The local cerebral ischemia /reperfusion model was established by intraluminal thread occlusion of the middle cerebral arteries (MCAO), the middle cerebral arteries of rats were occluded for 2 hours and reperfused for 1, 3 and 7 days. The animals were divided into pseudo surgery group(sham group), model group, Yiqi group, Huoxue group and naoluo xintong group. Using the techniques of immuno-histochemical staining and in situ hybridization, the expression of Fas and FasL was observed in hippocampus CA1 area, the expression of Fas mRNA was also observed in the cortex of frontal and parietal lobe. RESULTS: A value of Fas and FasL protein expression or A value and positive unit of Fas mRNA expression in control group were higher than those in sham in hippocampus CA1 area, the cortex of frontal or parietal lobe after local cerebral ischemia/reperfusion in MCAO rats (P<0.01). A value and/or positive unit of their expression in naoluo xintong group were lower than those in control group (P<0.05 or P<0.01). A value and/or positive unit of their expression in Yiqi and Huoxue groups were higher than those in naoluo xintong group for 3 and/or 7 days (P<0.05 or P<0.01). CONCLUSION: naoluo xintong could resist neuron apoptosis, alleviate pathologic injury after local cerebral ischemia/reperfusion in MCAO rats by inhibiting the expression of Fas, FasL protein and Fas mRNA.  相似文献   

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9.
AIM: To investigate the effect of propofol on expression of protein kinase C (PKC) mRNA during pulmonary ischemia and reperfusion injury (PIRI) in rabbits. METHODS: Single lung ischemia and reperfusion animal model was used in vivo. The rabbits were randomly divided into three groups (n=9 in each): sham operated group (sham), PIR group (I-R) and PIR+ propofol group (PPF). Changes of several parameters including malondialdehyde (MDA), superoxide dismutase (SOD), wet to dry ratio of lung tissue weight (W/D) and index of quantitative assessment of histologic lung injury (IQA) were measured at 60 minutes after reperfusion in lung tissue. Meanwhile the location and expression of PKC mRNA were observed. Lung tissue was also prepared for light microscopic and electron microscopic observation at 60 minutes after reperfusion. RESULTS: As compared with group I-R, PKC mRNA strongly expressed in intima and extima of small pulmonary artery as well as thin-wall vessels (mostly small pulmonary veins) in PPF group. The average optical density values of PKC-α、δ and θ mRNA in small pulmonary veins PPF in group showed significantly higher than that in I-R group (all P<0.01). SOD increased and MDA, W/D and IQA decreased at 60 minutes after reperfusion in lung tissue (P<0.01 and P<0.05). Abnormal changes of the lung tissue in morphology were lessen markedly in PPF group. CONCLUSIONS: Propofol produces notable protective effects on PIRI in rabbits by activating PKC-α， δ and θ mRNA expression in lung tissue, raising NO level, dropping OFR level and decreasing lipid peroxidation.  相似文献   

10.
AIM: To investigate the effects of ethane 1,2-dimethanesulfonate (EDS) preconditioning on renal ischemia/reperfusion (I/R) injury in male Sprague-Dawley (SD) rats. METHODS: Male SD rats (n=48) were randomly assigned to 6 groups: blank, sham, I/R, EDS+I/R, EDS+testosterone (TST)+I/R, and castration (Cast)+I/R. The renal pedicles were bilaterally occluded with a microvascular clamp for 45 min to establish renal I/R-induced injury model. Bilateral orchiectomy was conducted 2 weeks before surgery. EDS (75 mg/kg) was intraperitoneally injected 5 d before operation. Blood samples were collected 24 h after reperfusion from the vena orbitalis posterior plexus. Luteinizing hormone (LH), TST, serum creatinine (SCr), blood urea nitrogen (BUN), and kidney injury molecule-1 (KIM-1) were detected. The renal tissues were harvested to measure the level of TNF-α and the expression of Fas mRNA and caspase-3 protein. RESULTS: Serum TST levels in EDS+I/R group and Cast+I/R group were below the minimum detectable threshold. Compared with other groups, the rats in EDS+I/R group and Cast+I/R group had higher levels of SCr, BUN and KIM-1 (P<0.05). SCr and BUN levels showed no significant difference between EDS+I/R group and Cast+I/R group (P>0.05), but KIM-1 level in EDS+I/R group was lower than that in Cast+I/R group (P<0.05). After reperfusion for 24 h, the levels of TST and LH in EDS+I/R group, Cast+I/R group and EDS+TST+I/R group were lower than those 1 h before operation (P<0.05). Compared with Cast+I/R and I/R group, the TNF-α level and expression of Fas mRNA and caspase-3 protein were significantly decreased in EDS+I/R group (P<0.05). CONCLUSION: EDS preconditioning substantially reduces the serum TST level, thus attenuating I/R-induced acute renal injury. TNF-α-induced Fas/FasL pathway may be involved in this process.  相似文献   

11.
AIM: To investigate the effects and mechanism of Le Er Mai (LEM) on the apoptosis of hippocampus neuronal cells in the anaphase of cerebral ischemic reperfusion injury in rats.METHODS: A rat model of middle cerebral artery occlusion reperfusion (MCAO) was produced with the intraluminal filament. During reperfusion for 30 d after 2 h of ischemia, the TUNEL staining methods were used to detect apoptosis of hippocampus neuronal cells, and immunohistochemical technique were employed to examine the protein expression of Fas, Bax, caspase-3 and caspase-9 in the hippocampial. The gene expressions of fas, bax, caspase-3 and caspase-9 in hippocampial were examined by RT-PCR. RESULTS: After 2 h ischemia and 30 d reperfusion, compared with sham-operated group, TUNEL-positive staining cells and expression levels of Fas, Bax as well as caspase-3 and caspase-9 obviously increased, and the mRNA expressions of fas, bax, caspase-3 and caspase-9 in hippocampial markedly up-regulated in model group. Compared with model group, LEM at dose of 2.00 g/kg or 0.87 g/kg, and flunarizinum significantly reduced apoptosis and decreased the protein expressions of Fas, Bax, caspase-3 and caspase-9 in hippocampial, and down-regulated the mRNA expressions of fas, bax, caspase-3 and caspase-9 (P<0.05), those action of LEM in 0.87 g/kg dosage group was lower than those in 2.00 g/kg dosage group.CONCLUSION: LEM obviously lower the injury of hippocampial in the anaphase of cerebral ischemia reperfusion through inhibiting the apoptosis of hippocampus neuronal cells. The mechanism of LEM may be related to regulate the expression of signal transduction pathway correlated gene of apoptosis in neuronal cells.  相似文献   

12.
AIM: To investigate the effects of delayed ischemic preconditioning on renal ischemia-reperfusion injury in mice and to study the role of hypoxia inducible factor 1α(HIF-1α). METHODS: Male C57/BL6N mice were randomly divided into 3 groups: sham operation group(sham), ischemia/reperfusion group(IR) and ischemic preconditioning group(IPC). Thirty-minute ischemia was induced by clamping renal bilateral pedicles followed by reperfusion in IR group. Fifteen-minute pre-ischemia was performed 4 days before IR in IPC group. Serum creatinine(Scr), blood urea nitrogen(BUN), kidney morphology and apoptosis were observed at different time points following reperfusion. The expression of HIF-1α in the renal tissues was evaluated by the methods of immunohistochemistry and Western blotting analysis. The mRNA expression of vascular endothelial growth factor(VEGF) and glucose transporter-1(Glut-1) was detected by real-time quantitative RT-PCR.RESULTS: Compared with IR group at 24 h following reperfusion, acute tubulointerstitial injury was significantly relieved in IPC group. The levels of Scr and BUN, and apoptosis of tubular epithelial cells were also decreased in IPC group. Nuclear expression of HIF-1α was higher in IPC group than that in IR group. The mRNA expression of VEGF and Glut-1, the target genes of HIF-1, was also increased significantly in IPC group. CONCLUSION: Delayed ischemic preconditioning attenuates both morphologic and functional injuries induced by renal ischemia/reperfusion. This protective effect may be related to the increased expression of hypoxia inducible factor.  相似文献   

13.
AIM: To study the effects of soybean isoflavones on mitochondrial ultrastructure, neuronal apoptosis and expression of cytochrome C, caspase-9 and caspase-3 in the rats with cerebral ischemia/reperfusion.METHODS: Adult healthy SD rats (n=60) were randomly divided into 3 groups: sham group, ischemia/reperfusion injury (I/R) group and soybean isoflavone (SI) pretreatment group. Soybean isoflavones (120 mg·kg-1·d-1) were fed by gastric lavage for 21 d. The global ischemia/reperfusion model of the rats was established by blocking 3 vessels, and then reperfused for 1 h after 1 h of ischemia. The morphological change of the cerebral cortex cells was observed under light microscope. The mitochondrial ultrastructure of the cerebral cortex cells was determined by transmission electron microscope. The apoptotic rate of the cerebral cortex cells was detected by flow cytometry. The expression of cytochrome C, caspase-9 and caspase-3 in the cerebral cortex cells was determined by semi-quantitative RT-PCR and immunohistochemical techniques.RESULTS: Disintegration of mitochondria membrane and disappearance of the mitochondrial cristae were seen in I/R group. Compared with I/R group, the change of ultrastructure of mitochondria was significantly improved by soybean isoflavone pretreatment, and the neuronal apoptotic rate was also significantly decreased (P<0.01). The mRNA expression and protein content of cytochrome C, caspase-9 and caspase-3 in I/R group were obviously higher than those in sham group (P<0.01). Compared with I/R group, the mRNA expression and protein content of cytochrome C, caspase-9 and caspase-3 in SI group were significantly decreased (P<0.01).CONCLUSION: Soybean isoflavones attenuate cerebral ischemia/reperfusion injury by stabilizing the structure of mitochondria, preventing cytochrome C release to the cytoplasm, inhibiting the activation of caspase-9 and caspase-3 and decreasing cell apoptosis．  相似文献   

14.
AIM: To explore the influence of polydatin (PD) on Toll-like receptor 4 (TLR4) signal transduction pathway during lung ischemia reperfusion injury in rabbits. METHODS: Rabbit lung model of ischemia reperfusion (IR) injury was constituted in vivo. Thirty rabbits were divided into groups randomly: control (C), IR and PD group, respectively. The concentration of endotoxin (ET) in plasma was analyzed by end-point chromogenic assay. The protein expressions of TLR4, nuclear factor (NF)-κB p65 and heat shock protein 70 (HSP70) were measured by immunohistochemistry. The intracellular adhesion molecule-1 (ICAM-1) mRNA expression was detected by in situ hybridization histochemistry. The ultrastructural changes were observed by electron microscope. RESULTS: No significant difference of ET concentration in plasma between groups (all P>0.05) was observed. The protein expressions of TLR-4, NF-κB p65, HSP70 and ICAM-1mRNA in IR group were significantly increased as compared to C group and PD group, while those expressions in PD group were evidently higher than those in C group (all P<0.01). The lung pathological injuries in PD group were obviously alleviated as compared to IR group under electron microscope. CONCLUSION: It suggests that lung ischemia reperfusion releases endogenous ligands of TLR4 as HSP70, then activates NF-κB, promotes the release of mediators of inflammation such as ICAM-1. PD might have a protective effect on lung ischemia reperfusion injury by regulating TLR4 signal transduction pathway.  相似文献   

15.
AIM: To observe the expression and interrelationship of apoptosis controlling genes and proteins Fas, FasL, caspase-3 in rats with acute pancreatitis (AP). METHODS: Forty male Sprague Dawley rats were randomly divided into four groups, 10 rats each group. Acute pancreatitis with different inflammatory degree was induced by retroinjecting 2.0%, 3.5% or 5.0% sodium taurocholate at dose of 1 mL/kg body weight into the pancreaticobiliary duct. All the rats were sacrificed 6 h after operation. The pathologic changes of pancreas were observed under optical microscope. The protein and mRNA expressions of Fas, FasL, caspase-3 in pancreatic tissue were measured by Western blotting and RT-PCR. The apoptosis of acinar cells was measured by the methods of in situ end labeling. RESULTS: In normal pancreatic tissue, there appeared the protein and mRNA expression of Fas, FasL, caspase-3. In acute pancreatitis with different inflammatory degree, with the degree of inflammation worsen, the apoptosis cells tapered, the expression of above protein and mRNA also descended gradually. Furthermore, the variation tendency of caspase-3 among the four groups was in coincidence with Fas or FasL. CONCLUSION: Fas/FasL -mediated apoptotic pathway participates in the regulation of acinar cell apoptosis in acute pancreatitis.  相似文献   

16.
AIM: To investigate the protective effects of ischemic post-conditioning on the expression of early growth response factor 1 (Egr-1) and interleukin-1β(IL-1β) in ischemia-reperfusion injured lung in rats. METHODS: The model of lung ischemia-reperfusion injury was established in 24 rats and the rats were randomly allocated to 3 different groups (n=8 in each group): (1) sham group: only sham operation (thoracotomy) and no ischemia for 3 h; (2)ischemia-reperfusion group (I/R group): interruption of pulmonary perfusion and ventilation for 1 h followed by reperfusion for 2 h; (3) ischemic post-conditioning group (IPostC group): ischemic post-conditioning (5 min of reperfusion and 5 min of ischemia for 3 times) between the end of ischemia and the beginning of the reperfusion followed by reperfusion for 1.5 h. The lung tissues (prepared to small pieces of about 20 mg) were collected and homogenized at the end of the experiment. The concentration of myeloperoxidase (MPO) in the homogenate was determined. The wet to dry weight ratio (W/D) of the lung tissues was also measured at the end of reperfusion. The pathological changes of the lung tissues were observed under light microscope after reperfusion. The mRNA expression of Egr-1 and IL-1β in the lung tissues was detected by RT-PCR. RESULTS: Compared with sham group, the mRNA expression of Egr-1 and IL-1β, the levels of MPO and W/D were significantly increased in I/R group (P<0.05). The inflammatory responses of the lungs in I/R group were significantly severer than those in sham group. Compared with I/R group, the mRNA expression of Egr-1 and IL-1β, the levels of MPO and W/D in IPostC group were significantly decreased (P<0.05). The inflammatory responses of the lungs in IPostC group were also significantly attenuated. CONCLUSION: Ischemic post-conditioning significantly reduces ischemic reperfusion injury of the lung by inhibiting the expression of Egr-1 and IL-1β.  相似文献   

17.
AIM:To investigate the effect of L-arginine (L-Arg) on expression of bcl-2, bax mRNA during pulmonary ischemia and reperfusion injury (PIRI) in rabbits.METHODS:Single lung ischemia and reperfusion animal model was used in vivo. The rabbits were randomly divided into three groups: sham operated group (sham, n=12), ischemia-reperfusion group (I/R, n=12) and I/R+ L-arginine group (L-Arg, n=12). Changes of several parameters, which included apoptotic index (AI), wet to dry ratio of lung tissue weight (W/D) and index of quantitative assessment of histologic lung injury (IQA), were measured at 300 min after reperfusion in lung tissue. Meanwhile the location and expression of bcl-2, bax mRNA as well as the ratio of bcl-2 mRNA/bax mRNA were observed. The lung tissue was prepared for light microscopic and electron microscopic observation at 60, 180 and 300 min after reperfusion. RESULTS:As compared with I/R group, in intima and extima of small pulmonary artery, alveoli, and bronchiole epithelia, the expression of bcl-2 mRNA and the ratio of bcl-2 mRNA/bax mRNA were increased, and the expression of bax mRNA was decreased in L-Arg treatment group. The values of AI, W/D and IQA showed significantly lower than that in I/R group at 180 minutes after reperfusion in lung tissue (P<0.01 and P<0.05). Meanwhile, abnormal changes of the lung tissue in morphologically were markedly lessened in L-Arg treatment group.CONCLUSION:L-arginine produces a notable protective effect on PIRI in rabbits by up-regulating bcl-2 mRNA expression, down-regulating bax mRNA expression in lung tissue and regulating the balance of bcl-2 mRNA and bax mRNA to decrease apoptosis.  相似文献   

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19.
AIM: To study the change of myocardial ceramide during myocardial ischemia/reperfusion and the relationship between ceramide and apoptosis and oxidative stress. METHODS: After inducing myocardial ischemia/reperfusion (I/R) injury in mice with pituitrin (Pit), myocardial SOD activity and MDA content were measured. DNA agarose gel electrophoresis and fluorescent staining of DAPI were done to check up apoptosis. The content of myocardial ceramide (μg/kg) was measured through HPTLC and scan of thin plate. RESULTS: The myocardium of I/R model group had the phenomenon of DNA ladder. Apoptosis index and ceramide content in I/R model group were higher than those in normal control group (P<0.01). SOD activity in I/R modal group was lower than that in normal control group (P<0.01). The apoptosis index and ceramide content in I/R model group were positive correlative (r=0.970，P<0.01). The myocardial content of ceramide and MDA were positively correlative too (r=0.974, P<0.01). CONCLUSION: The results indicate that there are apoptosis, oxidative stress and increase in ceramide content in ischemia/reperfusion myocardium.  相似文献   

20.
AIM: To study the alteration and role of apelin in myocardial ischemic preconditioning and ischemia/reperfusion injury of rats.METHODS: Forty-five SD rats were randomly divided into three groups: ischemia/reperfusion group (IR),ischemia pre-conditioning group (IP) and sham operation group.ECG was continuously used to evaluate the score of arrhythmias.The protein levels of apelin-36 in myocardium and plasma were detected by radioimmunoassay.The expression of apelin was observed by immunohistochemistry.RESULTS: (1) The scores of arrhythmias in IP group (2.1±0.5) was only 58.3% of IR group (3.6±0.8) ( P<0.01).(2) The apelin-36 protein level of plasma and myocardium in IR group were respectively lower by 36.1% and 45.6% than those in SH group (P<0.01),and those in IP group were lower by 23.8% and 24.7% than those in SH group (P<0.01),but higher than those in IR group (18.9% and 38.5%,respectively,P<0.05).(3) The staining absorbance of apelin in IR,SH and IP group was (7.87±2.41),(22.53±2.54) and (14.23±2.15),respectively.There were significant differences between IR and SH (P<0.01) and between IP group and SH group (P<0.05).(4) The scores of arrhythmias in IP and IR were negatively correlated with the protein level of apelin-36 in myocardium (r= 0.847,P <0.01).CONCLUSION: The down-regulation of apelin-36 in the plasma and myocardium of rats indicates that apelin has an important role in myocardial ischemic preconditioning and ischemia/reperfusion injury.  相似文献   

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