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1.
AIM: To evaluate the influence of maternal limb ischemic preconditioning (LIP) on the apoptosis of fetal hippocampal neurons induced by intrauterine distress-reoxygenation in rats. METHODS: Intrauterine ischemia was induced by clamping the uterine and uterine branch of the ovarian blood vessels with aneurysm clamps for a period of 15 min followed by removal of the clamps to permit reperfusion. Sprague-Dawley (SD) rats (n=12) were randomly divided into 4 groups on the 19th pregnant day: sham (S) group, LIP group, fetal distress (FD) group and LIP+FD group. The cesarean birth occurred on embryonic day 21 to obtain 12 fetal rats alive in each group. The fetal rats were decapitated and the pyramidal cells in CA1 hippocampus were observed under light microscope. The neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining and the apoptotic rate was calculated. The expression of Bcl-2 and Bax were detected by immunohistochemical method and Western blotting. RESULTS: The rates of neuronal apoptosis in FD group and LIP+FD group were significantly higher than that in S group (P<0.05), while no significant difference was observed between S group and LIP group (P>0.05). The expression of Bcl-2 and Bax in FD group and LIP+FD group was significantly higher than that in S group (P<0.05), while no significant difference was observed between S group and LIP group (P>0.05). The ratio of Bcl-2/Bax was lower in FD group than that in S group. Compared with FD group, the rate of neuronal apoptosis was significantly lower (P<0.05), while the ratio of Bcl-2/Bax was significantly higher (P<0.05) in LIP+FD group. CONCLUSION: Maternal limb ischemic preconditioning attenuates the apoptosis of fetal hippocampal neurons induced by intrauterine distress-reoxygenation in rats, which may be associated with the up-regulation of Bcl-2 expression.  相似文献   

2.
ATM: To investigate the influence of urocortin-I (Ucn I) preconditioning on the myocardial mitochondrial respiratory function and enzyme activity in the rats with ischemia reperfusion, and to observe the changes of ATP content in the myocardial cells. METHODS: (1) The healthy male Sprague-Dawley rats were randomly divided into 4 groups:normal group (Nor group), ischemia reperfusion group (IR group), Ucn I preconditioning group (Ucn I group), 5-hydroxy acid (5-HD)+Ucn I group. Langendorff perfusion was used to establish the in vitro model of cardiac ischemia reperfusion. At the end of the balance (T1), before ischemia (T2) and at the end of the reperfusion (T3) respectively, the myocardial mitochondria was extracted, the mitochondrial respiratory function and respiratory enzyme activity in each group were determined. (2) The method of MPA isolated heart perfusion was used to isolate myocardial cells of the adult rats. After cultured for 24 h, myocardial cells were divided into 4 groups:Nor group, hypoxia/reoxygenation group (I/R group), Ucn I group, 5-HD+Ucn I group. Hypoxia/reoxygenation model of myocardial cells was established. At the end of reoxygenation, the changes of myocardial ATP content were measured by high performance liquid chromatography.RESULTS: (1) Compared with T1, T2 time points, the respiratory function (state 3 respiratory rate, respiratory control rate) and NADH oxidase, succinate oxidase and cytochrome C oxidase activities at T3 time point were significantly decreased (P<0.05) in all groups except Nor group. At T3 time point, the myocardial mitochondrial respiratory function and respiratory enzyme activity in Ucn I group were superior to 5-HD+Ucn I group and IR group (P<0.05), but was inferior to Nor group (P<0.05). At T3 time point, the respiratory function of myocardial mitochondria and respiratory enzyme activities (NADH oxidase, succinate oxidase) in 5-HD+Ucn I group were better than those in IR group (P<0.05), but no statistical difference of the cytochrome C oxidase activity between the 2 groups was observed. The respiratory function and 3 kinds of respiratory enzyme activities at T1, T2 time points had no statistical change. (2) At the end of the reoxygenation, the myocardial ATP content in Nor group was higher than that in other groups (P<0.01). The myocardial ATP contents in I/R group and 5-HD+Ucn I group were lower than that in Ucn I group (P<0.05). In additon, 5-HD+Ucn I group was higher ATP content compared with I/R group (P<0.05). CONCLUSION: Ucn I preconditioning attenuates the ischemia/reperfusion induced damages of myocardial mitochondrial respiratory function and respiratory enzyme activity, thus ensuring the myocardial ATP contents under the condition of hypoxia/reoxygenation.  相似文献   

3.
AIM: To investigate the effects of heptanol preconditioning on the changes of structure, function and connexin 43 (Cx43) content in mitochondria in a rabbit model of myocardial isehemia-reperfusion (IR) injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h. Sixty-four rabbits were randomly divided into 4 groups (n=16 in each group): sham operation group (sham group), ischemia-reperfusion group (IR group), ischemic preconditioning group (IP group) and heptanol preconditioning group (HT group). All rabbits in the 4 groups were killed 4 h after reperfusion. Myocardial infarct size was determined at the end of the experiment. Mitochondria was isolated by centrifugations. The ultrastructural changes of the mitochondria were observed under electronic microscope. The mitochondrial membrane potential, Ca2+ concentration, MDA content and SOD activity of myocardial mitochondria were also examined. The content of mitochondria Cx43 was detected by Western blotting. RESULTS: Compared to IR group, the myocardial infarct size was significantly reduced in IP (18.97%±2.80%) and HT (19.97%±3.80%) groups, the damage of mitoehondrial ultrastructure was milder (P<0.05), mitochondrial membrane potential was significantly higher and Ca2+ concentration was much lower (P<0.01) in IP group and HT group. No significant difference of MDA content and SOD activity in myocardial mitochondria between IR group and HT group was found. However, MDA content were much lower and SOD activity was significantly higher in IP group as compared to IR group (P<0.01). Compared to sham group, the mitochondria Cx43 expression was distinctly decreased compared to IR group (P<0.05) and no significant difference was found between IP group and HT group (P>0.05). CONCLUSION: Heptanol preconditioning protects myocardium from ischemia-reperfusion injury. The mechanism may be related to increasing in mitochondrial membrane potential, alleviating Ca2+ overload in myocardial mitochondria and attenuating the decrease in mitochondria Cx43 expression induced by isehemia-reperfusion.  相似文献   

4.
AIM: To study the effect of L-arginine (L-Arg) on function and structure of mitochondria in ischemia-reperfusion (MRI) myocardial cells. METHODS: Thirty rabbits were randomly divided into three groups (n=10 in each), control group, MIR group and MIR+L-Arg group. The mitochondrial respiratory function, Ca2+ concentration ([Ca2+]m), malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. Meanwhile, the contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), total adenylic acid number (TAN) and energy charge (EC) in the myocardial tissue were respectively measured. Moreover, the ultrastructure changes in myocardial mitochondria were observed during MIR. RESULTS: The mitochondrial respiratory control rate (RCR), velocity 3 (V3), SOD, surface density (Sv) and specific surface (δ) in MIR+L-Arg group were higher than those in MIR group, velocity 4 (V4), [Ca2+]m, MDA, volume density (Vv), horizental diameter (Hd) were lower than those in MIR group. ATP, ADP, TAN and EC levels of myocardial tissue were higher than those in MIR group. There was no significant difference between MIR+L-Arg and control group in V3, V4, SOD, MDA, Vv, Sv, δ, Nv, Vd, AMP and TNA. CONCLUSION: It is suggested that L-Arg improves the function and structure of mitochondria in myocardial cells in the reperfusion injury after myocardial ischemia by decreasing oxygen free radical level and Ca2+ overload in the mitochondria.  相似文献   

5.
AIM: To observe the effect of preconditioning with pioglitazone on ischemia reperfusion/hypoxia reoxygenation-induced mitochondrial ultramicro-structure and membrane potential in rats. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham-operated (SO) group, ischemia reperfusion (IR) group, pioglitazone preconditioning group (Pio-P) and 5-HD+pioglitazone (5-HD+Pio) group. Apart from the SO group, IR, Pio-P and 5-HD+Pio groups were subjected to 30 min ischemia and 4 h reperfusion. The heart was quickly removed for observing the structure of mitochondria and measurement of the apoptosis index (AI) by TUNEL. Primary cultured cardiomyocytes of Sprague-Dawley rats were divided into control, hypoxic reoxygenation (HR) and different concentrations of Pio-P group. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (ΔΨm). RESULTS: The injury of mitochondrial structure in IR group was severer than that in Pio-P group, while the difference between 5-HD+Pio group and IR group was not evident. Flameng score in Pio-P group(1.62±0.60) was significantly lower than that in IR group (2.75±1.09), P<0.01. AI in Pio-P group (28.19%±4.93%) was lower than that in IR group (55.44%±6.63%),P<0.05. The rates of low ΔΨm cells in (5 μmol/L,10 μmol/L and 15 μmol/L) Pio-P group were (45.89±3.63)%, (17.13±1.37)% and (18.43±2.44)%, significantly lower than that in HR group (56.52%±2.87%),P<0.05, while the difference between 10 μmol/L group and 15 μmol/L group was not significant (P>0.05). CONCLUSION: Pioglitazone protects the heart from ischemia reperfusion/ hypoxia reoxygenation injury evidenced by improving mitochondrial ultrastructure and lessening the loss of mitochondrial membrane potential, and decreasing apoptosis. The cardioprotective effects can be inhibited by the blocker of mitochondrial ATP-sensitive potassium channels.  相似文献   

6.
AIM:To explore the effects of genipin (GEN) on high glucose (HG)-induced oxidative stress injury and apoptosis in H9c2 cardiomyocytes.METHODS:H9c2 cells were cultured in vitro and HG-induced injury model was established. H9c2 cells were divided into 4 groups:normal control (NC) group (glucose at 5.6 mmol/L), HG group (glucose at 50 mmol/L), NG+GEN group and HG+GEN group. The concentration of genipin was used at 10 μmol/L. The viability of the H9c2 cells was measured by CCK-8 assay. The intracellular malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined by enzyme labeling and WST-1 methods, respectively. The activity of lactate dehydrogenase (LDH) in the cell culture supernatant was detected by microplate method. Fluorescent probe DCF was used to detect intracellular levels of reactive oxygen species (ROS). Nucleosome fragments was measured to evaluate cell apoptosis by ELISA. The intracellular mitochondrial membrane potential was detected by JC-1 method. The protein levels of Mn-SOD, cytochrome C (Cyt C), Bax and cleaved caspase-3 were determined by Western blot. RESULTS:Compared with HG group, the cell viability in HG+GEN group was increased significantly (P<0.05), the levels of MDA and LDH were decreased (P<0.05), SOD activity was increased (P<0.05), the levels of ROS and nucleosome fragments in HG+GEN group were decreased (P<0.05), and the mitochondrial membranes potential was notably increased (P<0.05). Compared with NG group, the activation of Mn-SOD was decreased, but the protein levels of Cyt C, Bax and cleaved caspase-3 were increased in HG group (P<0.05). Compared with HG group, the activation of Mn-SOD was increased, and the protein levels of Cyt C, Bax and cleaved caspase-3 were decreased in HG+GEN group (P<0.05).CONCLUSION:Genipin protects HG-induced H9c2 cardiomyocytes against oxidative stress injury and apoptosis.  相似文献   

7.
AIM: To observe the effects of sevoflurane preconditioning on brain injury in hypoxic mice and its possible mechanism. METHODS: Male C57BL/6J mice were randomly divided into control (C) group, hypoxia (H) group, 2% sevoflurane preconditioning for 30 min + hypoxia (S1+H) group, 2% sevoflurane preconditioning for 60 min+hypoxia (S2+H) group and 4% sevoflurane preconditioning for 30 min + hypoxia (S3+H) group. The hypoxia model was established by continuous inhalation of (6.5±0.1)% O2 for 24 h. The sevoflurane preconditioning treatments, S1, S2 and S3, were conducted by inhalation of 2% sevoflurane for 30 min, 2% sevoflurane for 60 min and 4% sevoflurane for 30 min, respectively, with the carrier of (21.0±0.5)% O2, followed by washout for 15 min and then hypoxia treatment. The histological changes of the hippocampal CA1 area were observed under light microscope and transmission electron microscope (TEM), and serum lactate dehydrogenase (LDH) activity was measured by colorimetric method. Furthermore, the protein levels of erythropoietin (EPO) and vascular endothelial growth factor (VEGF) in brain tissue homogenate were examined by ELISA, and the content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured by microplate reader. RESULTS: After hypoxia for 24 h, cell edema or pyknosis in the hippocampal CA1 area was observed in H group. Sevoflurane preconditioning reduced hypoxic injury, and the cell ultrastructure under TEM was significantly improved in S2+H group. Compared with C group, the serum LDH activity and the levels of EPO, VEGF and MDA in brain tissues were significantly increased in H group, while the activity of SOD and GPx decreased. After sevoflurane pretreatment, the serum LDH activity and the levels of EPO and VEGF in brain tissues were lower than those in H group, and the most significant difference was observed in S2+H group. Moreover, the MDA content and SOD activity decreased, and the GPx activity increased in the sevoflurane preconditioning groups. CONCLUSION: Sevoflurane preconditioning attenuates brain injury in hypoxic mice by regulating antihypoxic protein synthesis and reducing oxidative stress.  相似文献   

8.
AIM: To investigate the effects of Ganoderma lucidum spores on superoxide dismutase(SOD),malondialdehyde(MDA),total antioxidative capacity(T-AOC), cytochrome C, heat-shock protein 70 (HSP70), mitochondrial Ca2+ and brain-derived neurotrophic factor(BDNF) in the brain tissues of epilepsy rats.METHODS: The rat chronic epilepsy model was by intraperitoneal injection of pentetrazole(PTZ) at a subconvulsant dose (32 mg/kg).Flame atomic absorption method was used to detect the content of mitochondrial Ca2+,and spectrophotometer colorimetry was used to measure SOD activity,MDA content,T-AOC and cytochrome C levels in rat brain tissues. HSP70 and BDNF were determined by immunohistochemical method.RESULTS: The contents of mitochondrial Ca2+ and cytochrome C were higher, and the content of intracytoplasmic cytochrome C in the rat brain tissues was obviously lower in Ganoderma lucidum spores group than that in epileptic model group. Compared to epileptic model group, the activity of SOD and T-AOC in cytoplasm of the rat brain tissues decreased while MDA increased, and the numbers of BDNF-positive cells in cerebral cortex and hippocampus were significantly increased in Ganoderma lucidum spores group. The positive neuron population of HSP70 in hippocampus, basal nucleus and cortex was significantly higher in Ganoderma lucidum spores group than that in epilepsy model group.CONCLUSION: Ganoderma lucidum spores attenuate the impairment of neuronal mitochondria induced by seizure, and accelerate the expression of BDNF, resulting in restoring the energy metabolism in mitochondrion, thus alleviating the impairment and apoptosis of the brain tissues.  相似文献   

9.
AIM:To investigate the effects of prenatal stress (PS) on neurons and neuronal ultrastructure of hippocampus in offspring rats, and to explore the role of the overproduction of oxidants. METHODS:One month male offspring rats were obtained to observe the neuronal number, neuronal ultrastructure and the number of nNOS -positive cell in hippocampus. RESULTS:The neuronal number of CA1 and CA4 subregions in late gestation stress (LS) offspring decreases significantly. The neuronal ultrastructure of CA1 subregion in MS (stress in 7-13 days of gestation) and LS offspring appeared bulgy mitochondria, unclear membrane and irregular electron density. Lipofuscin pigments increased; The number of nNOS-positive cell in CA1, CA2, CA3 subregions and DG of MS group and the whole hippocampus of LS group increased significantly. CONCLUSION:PS damaged the neurons and neuronal ultrastructure of hippocampus of offspring rats. The damages were associated with the overproduction of oxidants.  相似文献   

10.
AIM: To study the protective effect of ischemia preconditioning (IPC) on ischemia/reperfusion (IR)-damaged myocardium in young and old rats. METHODS: Male Wistar rats aged at 3 months (young) and 20 months (old) were used to establish myocardial IPC model and IR model with the method of Langendorff heart perfusion. The rats were divided into young ischemia/reperfusion (YIR) group, young ischemic preconditioning (YPC) group, old ischemia/reperfusion (OIR) group and old ischemic preconditioning (OPC) group. Transmission electron microscopy was used to observe the ultrastructural changes of myocardial tissue and myocardial mitochondria. The myocardial infarction area was determined by TTC staining. The lactate dehydrogenase (LDH) content in coronary effluent fluid and the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardial tissues were detected by the method of colorimetry. The levels of nitrated and carbonylated proteins in myocardial tissue were measured by ELISA. The myocardial cell apoptosis was analyzed by TUNEL assay. The mitochondrial respiratory function and mitochondrial permeability transition pore opening induced by calcium load were evaluated by oxygen electrode method. RESULTS: Compared with YIR group, the myocardial infarction area in YPC group was obviously smaller, SOD activity in myocardial tissues increased, LDH activity in coronary effluent fluid and the content of MDA decreased, and the levels of nitrated and carbonylated proteins in the cardiac tissues reduced. In YPC group, the mitochondrial membrane structure appeared intact, cristae of the mitochondria showed close arrangement, and the matrix was compressed under the electron microscope. Myocardial mitochondrial respiratory control rate, state Ⅲ oxygen consumption and the P/O ratio in YIR group all significantly increased, proton leak decreased, mitochondrial swelling induced by calcium distinctly reduced, and myocardial apoptosis rate declined. No significant difference of the above indexes between OIR group and OPC group was observed. Compared with YPC group, myocardial ultrastructural damage increased clearly, cardiac oxidative stress increased, mitochondrial respiratory function declined, and cell apoptosis and necrosis increased in OPC group. CONCLUSION: Ischemic preconditioning has protective effect against myocardial IR injury in young rat hearts, while old rat hearts were less sensitive to ischemic preconditioning, leading to bluntness of cardioprotection with IPC in aging hearts. This may be related to mitochondrial injury and severe cellular apoptosis caused by increase of cardiac oxidative stress levels in the aging ischemic preconditioning heart.  相似文献   

11.
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12.
AIM：To investigate the effects of cyclosporin on oxidative stress and mitochondrial energy metabolism in the rat hippocampus after status epilepticus. METHODS：Status epilepticus was induced by pilocarpine. The changes of malondialdehyde and superoxide dismutase in the rat hippocampus with or without cyclosporin injection were evaluated. Additionally, the mitochondrial permeability transition, the activity of mitochondrial respiratory chain complex I/III and ATP content in the rat hippocampus were detected. RESULTS：Cyclosporin significantly inhibited mitochondrial permeability transition in the rat hippocampus after status epilepticus. Decreased malondialdehyde and increased superoxide dismutase levels were detected in cyclosporin treatment group compared with status epilepticus group (P<0.05). More-over, the activity of mitochondria respiratory chain complex I, not III, in the mitochondrial fraction increased after cyclo-sporin treatment (P<0.05). In addition, cyclosporin significantly prevented the decrease of ATP content in rat hippocampus after status epilepticus (P<0.05). CONCLUSION：Cyclosporin suppresses oxidative stress in the rat hippocampus after status epilepticus. Cyclosporin alleviates the impairment of mitochondrial energy metabolism in rat hippocampus after status epilepticus.  相似文献   

13.
AIM: To examine the effects of L-carnitine on apoptosis and oxidant injury in cultured neonatal rat cardiomyocytes induced by hypoxia/reoxygenation and its possible mechanism. METHODS: The cultured cardiomyocytes were divided into three groups， control， A/R group （anoxia for 120 min, reoxygenation for 240 min） and L-carnitine treatment group, in which cells were exposed to 20 mg/L, 50 mg/L, 100 mg/L, 200 mg/L L-carnitine respectively at 2 h before anoxia. The superoxide dismutase (SOD), succinate dehydrogenase (SDH) activities and malondialdehyde (MDA) content were examined, and the apoptosis was determined by flow of cytometry (FCM). In addition, the ultrastructure was observed by transmission electron microscopy. RESULTS: In A/R group, SOD and SDH activities were lower, the apoptosis rate and MDA content were higher than those in control group (P<0.05). In L-carnitine treatment group, SOD and SDH activities were higher, the apoptosis rate and MDA content were lower than those in A/R group, a L-carnitine concentration-dependent effect was found. Moreover, impairment of myocardial ultrastructure was more severe in A/R group than L-carnitine treatment group. CONCLUSION: L-carnitine can protect cardiomyocytes against hypoxia/reoxygenation-induced injury in a dose-dependent manner.  相似文献   

14.
AIM: To investigate the effects of glucagon-like peptide-1 (GLP-1) on myocardial ischemia-reperfusion (IR)/hypoxia-reoxygenation (HR) injury in rats. METHODS: Sprague-Dawley rats were randomly divided into 5 groups: sham group, IR group and IR+GLP-1 (0.03 nmol/L, 0.16 nmol/L and 0.30 nmol/L) groups. IR group and IR+GLP-1 group were subject to 30 min of ischemia and 3 h of reperfusion. The myocardial infarct size, the ultrastructural changes of the myocardial tissues, the apoptosis of the cardiomyocytes, the activity of superoxide dismutase (SOD) and the concentration of malondialdehyde (MDA) were detected. Primarily cultured cardiomyocytes were divided into 5 groups at random: control group, HR group and HR+GLP-1 (1 μmol/L, 5 μmol/L and 10 μmol/L) groups. The morphology and apoptosis of the cardiomyocytes were observed. The levels of lactate dehydrogenase (LDH),MDA,SOD,reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) in different groups were detected. RESULTS: Compared with IR group, the myocardial infarct size and cardiomyocyte apoptosis were remarkably reduced, mitochondrial ultrastructures were improved, the activity of SOD was increased and the concentration of MDA was decreased in IR+GLP-1 (0.03 nmol/L, 0.16 nmol/L and 0.30 nmol/L) groups. Compared with HR group, GLP-1 (1 μmol/L, 5 μmol/L and 10 μmol/L) preconditioning significantly decreased the myocardial injury, increased SOD activity, decreased MDA concentration and ROS production, and heightened MMP in a dose-dependent manner. CONCLUSION: GLP-1 protects cardiomyocytes from IR/HR injury, which may be partially due to the effects of anti-oxidative mechanism and the function of mitochondrial protection.  相似文献   

15.
AIM: To investigate the effect of polysaccharide from Fructus corni(PFC) on cardiomyocytes against hypoxia/reoxygenation (H/R) injury and its possible relationship with ROS/PKC/p38 MAPK pathway.METHODS: Primary cardiomyocytes were isolated from neonatal SD rats and randomly divided into normal group, H/R group, PFC (20 mg/L, 100 mg/L and 200 mg/L) preconditioning+H/R groups, chelerythrine+PFC (100 mg/L)+H/R group and SB203580+PFC (100 mg/L)+H/R group. The cell viability was measured by inverted microscopic observation. Apoptosis in the cardiomyocytes was detected by Hoechst 33258 staining and fluorescence microscopy. The levels of lactate dehydrogenase (LDH) and superoxide dismutase (SOD) in the cell culture supernatants, and the reactive oxygen species (ROS) in the cells were also measured by microplate reader. The protein levels of PKC, p-p38 MAPK and HSP70 in the cells were detected by Western blotting.RESULTS: Compared with normal group, the cell viability and beating frequency were decreased in H/R group. LDH and ROS contents, apoptotic rate and p-p38 MAPK level increased significantly (P<0.01). Compared with H/R group, PFC preconditioning increased beating frequency, SOD activity and the protein level of PKC and HSP70, and decreased ROS production, the protein level of p-p38 MAPK and cell apoptotic rate. However, the effect of PFC was inhibited by chelerythrine or SB203580.CONCLUSION: PFC may protect cardiomyocytes from hypoxia/reoxygenation injury. Its mechanism is possibly involved in the inhibition of ROS via increasing the activity of SOD and the activation of PKC, and suppression of excessive activation of p38 MAPK.  相似文献   

16.
AIM:To observe the protective effect of non-wounded ischemic preconditioning on ischemic/reperfusion injury in isolated rat hearts. METHODS: 25 male SD rats, weighting (250±30) g, were randomly divided into three groups: control group (C,n=8), anoxia/reoxygenation group (A,n=8) and non-wounded legs ischemic preconditioning group (N-WIP,n=9).Hearts were isolated from rats and perfused on a Langendorff apparatus with a normal Krebs-Henseleit buffer (saturation 95% O2+5% CO2) at a constant pressure (8.33 kPa) and temperature (37 ℃) in C group; Following 15 min equilibration, hearts were subjected to 15 min of global ischemia and 15 min reperfusion (37℃) in A group; Rats were subjected to non-wounded leg repeated-brief ischemic preconditioning, and then treated in procedure similar to A group in N-WIP group.The activities of superoxide dismutase (SOD) and Ca2+-Mg2+-ATPase, malondialdehyde (MDA) content of efflux from coronary vessel and myocardium, myocardium monophasic action potential and contractile force were measured before ischemia, 15 minutes after ischemia and 5, 15 minutes after reperfusion. RESULTS:Compared with A group, non-wounded legs ischemic preconditioning reduced the incidence of reperfusion arrhythmias (P＜0.05), decreased the content of MDA of myocardium (P＜0.01), enhanced the activities of SOD (P＜0.01) and stabilized myocardial membranous potential,the activity of Ca2+-Mg2+-ATPase and contractile function. CONCLUSION:These results indicate that non-wounded leg ischemic preconditioning has a protective effect on ischemia-reperfusion injury in isolated rat hearts. The mechanism may be related to the strength of antioxidation, the stability of Ca2+-Mg2+-ATPase activity and membranous structure in myocardium.  相似文献   

17.
AIM: The experiment was designed to study the effect of compound Danshen dripping pills (DSDP) on myocardium with anoxin/reoxygenation. METHODS: The myocardial anoxin/reoxygenation model was made in perfused isolated rat heart. DSDP and isosorbide dinitrate (ID) were given at the time of pre-perfusion and reperfusion, then HPLC and H-600 electron microscope were used to detect the change of high energy phosphate and the ultrastructure of myocardial cell. RESULTS: ① The contents of AMP, ADP, ATP and AN in myocardium in only anoxin/reoxygenation group were obviously lower than those in the control group (P<0.01).② The contents of AMP, ADP, ATP and AN in myocardium in the groups with DSDP were higher than those in only anoxin/reoxygenation group (P<0.01), also higher than those in the groups with ID (P<0.01). In the two groups with DSDP, the contents of ATP and AN were close to normal (P>0.05). ③ In the groups with ID, the contents of AMP, ADP, ATP and AN were distinctively lower than those in the control group (P<0.01). CONCLUSION: These results indicated that DSDP administration could significantly increase the content of high energy phosphate in myocardium with anoxin/reoxygenation and decrease the ultrastructure injury of myocardial cells, and its protective effect was better than ID.  相似文献   

18.
AIM：To investigate whether quercetin (Que) protects cardiomyocytes from anoxia/reoxygenation (A/R) injury through protein kinase C epsilon (PKCε) pathway. METHODS：Primary cardiomyocytes were isolated from neonatal SD rats and exposed to A/R (3 h of anoxia followed by 2 h of reoxygenation) as well as Que and/or εV1-2 (a selective PKCε inhibitor) preconditioning. The expression of PKCε in the cells was detected by Western blotting. The levels of lactate dehydrogenase (LDH) and creatine kinase (CK) in cell culture supernatants, the reactive oxygen species (ROS) and mitochondrial membrane potential in the cells, the opening of mitochondrial permeability transition pore (mPTP) and the cell viability and apoptosis were also measured. RESULTS：The expression of PKCε protein was significantly increased in the cardiomyocytes pretreated with 40 μmol/L Que 72 h before A/R (P<0.01 vs A/R group). Meanwhile, Que preconditioning could increase cell survival rate, decrease ROS production and cell apoptosis, alleviate the loss of mitochondrial membrane potential and inhibit the opening of mPTP induced by A/R injury (P<0.01 vs A/R group). However, pretreatment with Que and εV1-2 attenuated these protective effects of Que (P<0.01 vs Que+A/R group). CONCLUSION：One of the mechanisms underlying the cardioprotective effect of Que might be the increase in PKCε protein expression and the activation of its downstream pathway.  相似文献   

19.
AIM:To investigate the role of myocardial nuclear factor kappa B (NF-κB)and manganese superoxide dismutase (Mn-SOD) in the mechanism underlying cardioprotective effect of delayed preconditioning mediated by adenosine A1 receptor agonist R-phenylisopropyladenosine ( R-PIA). METHODS:Male Wistar rats were randomly divided into three groups(n=12), Group normal saline, Group R-PIA and Group R-PIA plus DPCPX (an adenosine A1 receptor antagonist). Twenty four hours after administration of above drug, left ventricular myocardial samples of 4 rats in each group were obtained for assessment of myocardial Mn-SOD content (ELISA) and NF-κB binding activity (EMSA). Eight rats in each group, 24 hours after pretreatment as above, were subjected to chest-open and subjected to 30 min of regional myocardial ischemia followed by 120 min of reperfusion, and then the hearts of the rats were isolated to determine the infarct size (TTC stain ). RESULTS: The infarct size in group R-PIA was significantly less than that in group normal saline (P＜0.01), and there was no significant difference between group R-PIA+DPCPX and group normal saline in infarct size (P＞0.05). Myocardial NF-kappa B binding activity and Mn-SOD content in group R-PIA were all higher than those in group normal saline. There was no significant difference between group R-PIA+DPCPX and group normal saline in NF-κB binding activity and Mn-SOD content (P＞0.05). CONCLUSIONS:This study suggested that there might be a close relationship between delayed preconditioning mediated by adenosine A1 receptor agonist R-PIA and myocardial nuclear factor-kappa B binding activity and Mn-SOD protein expression.  相似文献   

20.
AIM: To study the effect of mild hypothermia on energy metabolism and hydroxyl radical production as well as delayed neuronal death (DND) in hippocampus during cerebral ischemia/reperfusion in gerbils.METHODS: Forebrain ischemia was induced by occluding bilateral common carotid arteries with aneurysm clamps for 10 min in gerbils. The DND in hippocampal CA1 sector was assessed by histological examination, and hydroxyl radical, ATP (adenosine triphosphate), ADP (adenosine diphosphate),AMP (adenosine monophosphate) levels were determined by high performance liquid chromatography with electrochemical or ultraviolet detection. RESULTS: The number of survival neuronal in hippocampal CA1 sector in mild hypothermia + I/R group was more than that in I/R group after ischemia/reperfusion 96 h. The content of 2,3-DHBA (2,3- dihydroxybenzoic acid) in hippocampus in I/R group was much higher than those in sham operation and mild hypothermia + I/R group after reperfusion 6 h (P＜0.01), but there were no significant differences in 2,3-DHBA outputs among 3 groups 48 h and 96 h after reperfusion. There were no obvious differences in ATP, ADP, AMP level in hippocampus among 3 groups 6 h after reperfusion. However, the content of ATP,ADP,AMP in mild hypothermia + I/R group was much higher than those in I/R group 48 and 96 h after reperfusion (P＜0.01).CONCLUSION: Mild hypothermia can reduced DND by improving the cerebral energy metabolism during forebrain ischemia/reperfusion in gerbils.  相似文献   

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