scholarly journals EFFECTS OF ZIZIPHUS JUJUBE SUPPLEMENTATION ON PRO- AND ANTI-APOPTOTIC PROTEIN EXPRESSION IN NEUTROPHILS AFTER RESISTANCE EXERCISE

2020 ◽  
Vol 20 (3) ◽  
pp. 5-14
Author(s):  
S Tayebi ◽  
K Krüger ◽  
M Safakar ◽  
P Bahrami ◽  
G Tahmasb ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Caspase 3 ◽  
Acute Effect ◽  
Human Neutrophils ◽  
Acute Administration ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Apoptotic Protein ◽  
Exercise Induced ◽  
Neutrophils Apoptosis

Introduction. It is suggested that jujube might have beneficial effects on exercise-induced immune perturbations, specifically on neutrophils apoptosis regulation, but its cellular mechanism is unclear. Aim. The aim of this study was to investigate the acute effect of Ziziphus jujuba administration on pro- and anti-apoptotic protein levels in human neutrophils in response to a session of circuit resistance exercise (Ex). Material and Methods. Participants completed an Ex (75 % 1RM, 9 exercises, 3 sets). While one group received a placebo, the other group (Zj) was supplemented daily with jujube (0.5 gr/kg body weight suspended in 2.5cc distilled water) one hour before Ex. Results. Ex increased the neutrophil level of [Ca2+]i, calpain-1 and caspase-3 (p < 0.05) while a reduction of calpastatin and XIAP were observed (p < 0.05). Zj either suppressed the [Ca2+]i or reversed the calpastatin, calpain-1, XIAP, and caspase-3 responses (p < 0.01). Conclusions. The data indicate that a single session of intensive Ex induced apoptotic signaling in human neutrophils with the involvement of [Ca2+]i-calpastatin-calpain axis upstream caspase-3. Acute administration of jujube solution before exercise attenuated these effects probably by providing energy sources for neutrophils or by functioning as antioxidants.

scholarly journals Supplementation with Ziziphus Jujuba Suppresses Apoptosis Signals in Neutrophils after Acute Exercise

2021 ◽  
Vol 10 (2) ◽  
pp. 31-39
Author(s):  
Seyed Morteza Tayebi ◽  
◽  
Karsten Krüger ◽  
Farahnaz Ebrahimi ◽  
Abbas Izadi ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Repeated Measures ◽  
Caspase 3 ◽  
Acute Exercise ◽  
Exercise Session ◽  
Human Neutrophils ◽  
Significance Level ◽  
Protein Levels ◽  
Ziziphus Jujuba ◽  
Circuit Resistance

It is suggested that jujube might benefit exercise-induced immune fluctuations, specifically on neutrophils’ apoptosis regulation, but its cellular mechanism is unclear. This study aimed to investigate the effect of one-week supplemen- tation with Ziziphus jujuba on pro- and anti-apoptotic protein levels of neutrophils in response to a session of circuit resistance exercise. Fourteen young, healthy male students completed a session of circuit resistance exercise (75% 1RM, nine exercises, three sets) in two groups (n=7). While one group received a placebo, the other group was supplemented with jujube (0.5 g/kg body weight suspended in 2.5 cc distilled water) started a weekday before the exercise session. Blood samples were collected 30 minutes before, immediately, and two hours after the exercise. Neutrophils were col- lected and pro- (Calpain-1, Bax, Caspase-3) and anti-apoptotic (Calpastatin, XIAP) proteins measured with ELISA. In- tracellular calcium ([Ca 2+ ]i) was assessed using the Atomic Absorption/ Flame Emission method. Repeated-Measures ANOVA was used for the interaction effects of TIME×GROUP (3×2) at the significance level (p) of 0.05. The SPSS software was used for analyses. Levels of ([Ca 2+ ]i), expression of calpain-, and caspase-3 were increased in response to circuit resistance exercise (p<0.05). In contrast, supplementation with jujube suppressed these changes (p<0.01). The data indicate that a single session of intensive circuit resistance exercise elevated apoptosis signalling in human neutrophils with the involvement of [Ca 2+ ]i-Calpastatin-Calpain axis upstream caspase-3. Supplementation with the jujube solution attenuated cell death signalling, possibly by providing energy for neutrophils. Otherwise, the improvement of the anti- oxidant status might be protective against ROS-induced apoptosis during exercise.

scholarly journals Protective Effect of Standardized Extract ofGinkgo bilobaagainst Cisplatin-Induced Nephrotoxicity

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Jie Song ◽  
Dan Liu ◽  
Liang Feng ◽  
Zhenhai Zhang ◽  
Xiaobin Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Porcine Kidney ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Ros Accumulation ◽  
Proximal Tubular ◽  
Antitumor Compound ◽  
Caspase Cascade

Cisplatin (CDDP) is a potent antitumor compound widely used with a notably side effect of nephrotoxicity inducing oxidative stress and apoptosis in kidneys. Standardized extract from the leaves of theGinkgo bilobatrees, labeled EGb761 (EGb), has been available on the market for its beneficial effects. The purpose of this study was to investigate the ability of EGb to prevent the nephrotoxic effect of CDDP and the mechanisms involved. Our results showed that EGb treatment restored the levels of creatinine, BUN, MDA, NO, SOD, CAT, GPx, and GSSG/GSH ratio in kidneys after CDDP injection. EGb also exhibited a tendency to decrease the elevated NF-κB translocation and caspase-3 protein levels in CDDP-treated kidneys. We further used a porcine kidney proximal tubular epithelial (LLC-PK1) cell line, finding that EGb accordingly inhibited ROS accumulation and iNOS increase induced by CDDPin vitro. EGb also attenuated IκB degradation and p65 NF-κB phosphorylation triggered by CDDP in LLC-PK1 cells. But EGb failed to influence CDDP-stimulated caspase cascade. These findings suggested that EGb’s renoprotective effect might be mediated by not only its well-known antioxidant activity but also the anti-inflammatory activity.

Neuroprotective Effects of Trolox, Human Chorionic Gonadotropin, and Carnosic Acid on Hippocampal Neurodegeneration After Ischemiareperfusion Injury

2019 ◽  
Vol 14 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Asrin Babahajian ◽  
Arash Sarveazad ◽  
Fereshteh Golab ◽  
Gelareh Vahabzadeh ◽  
Akram Alizadeh ◽  
...  
Keyword(s):  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Ischemia Reperfusion ◽  
Carnosic Acid ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Ischemic Group ◽  
Apoptotic Protein ◽  
Complications Of Stroke

Introduction: One of the serious complications of stroke is memory impairment, which is considered as one of the complications of reperfusion of tissue. The present study was designed to compare the effect of administration of Trolox, carnosic acid and Human Chorionic Gonadotropin (HCG) immediately after reperfusion of the stroke tissue on the memory and hippocampal histology. Method: Ischemia-Reperfusion Model (IRI) was created by bilateral occlusion of the common carotid artery for 15 minutes and the first dose was administered immediately after reperfusion. 10 days after ischemia, passive avoidance memory test and apoptotic protein levels were evaluated. Results: Cerebral Ischemia perfusion reduced the time of latency in entering the dark box in the ischemic group. Administration of Trolox and HCG increased this latency time, while treatment with carnosic acid had no effect. Also, IRI significantly reduced the number of healthy cells in the hippocampus. Administration of Trolox, carnosic acid and HCG increased the number of healthy cells and decreased the expression of Caspase-3 and Bax, but significantly increased the expression of Bcl-2 compared to the ischemic group. Conclusion: Findings indicate the beneficial effects of HCG and Trolox on the improvement of memory and the number of healthy cells in the hippocampal region. It is worth noting that the amount of apoptosis in the hippocampus was significantly reduced by Trolox, HCG and Carnosic acid.

Coping with Exercise Induced Spatial Memory Improvement in Morphine Dependent Rats by Inhibiting Brain Derived Neurotrophic Factor (BDNF)

2021 ◽  
Author(s):  
Aboozar Zare ◽  
Vali Nowzari ◽  
Tahereh Karimi-Jashni
Keyword(s):  
Spatial Memory ◽  
Learning And Memory ◽  
Potential Method ◽  
Voluntary Exercise ◽  
Morphine Dependence ◽  
Spatial Learning And Memory ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Neurotropic Factor ◽  
Exercise Induced

Background: Addiction as a chronic disorder that requires long treatment. One way to treating this chronic disease is exercise. Chronic exposure to opiates impairs spatial learning and memory. Given the well-known beneficial effects of voluntary exercise on cognitive functions, we investigated whether voluntary exercise would ameliorate the cognitive deficits that are induced by morphine dependence. If an effect of exercise was observed, we aimed to investigate the possible role of hippocampal brain-derived neurotropic factor (BDNF) in the exercise-induced enhancement of learning and memory in morphine-dependent rats. Methods: The rats were injected with bi-daily doses (10 mg/kg, at 12 hr. intervals) of morphine over a period of 10 days of voluntary exercise. Following these injections, a water maze task was performed twice a day for 5 consecutive days, followed by a probe trial 2 days later. A specific BDNF inhibitor (TrkB-IgG chimera) was used to block the hippocampal BDNF action during the 10 days of voluntary exercise. Results: The voluntary exercise diminished the severity of the rats’ dependency on morphine. A blockade of the BDNF action blunted the exercise-induced improvement of spatial memory, hippocampal neuron counting and BDNF protein levels in the dependent rats. Our results indicate that voluntary exercise could be increase the expression of LTP by lowering the induction threshold for LTP in the DG of morphine-dependent rats. Conclusion: Thus, voluntary exercise might be considered as a potential method to ameliorate some of the deleterious behavioral consequences of the abuse of morphine and other opiates.

Abstract 390: Cardiovascular Effects of the Angiotensin-(1-7) Analogue A1317

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Janaina F Braga ◽  
Neiva Caldeira ◽  
Roberto Q Lautner ◽  
Rodrigo A Fraga-Silva ◽  
Robson A Santos
Keyword(s):  
Arterial Pressure ◽  
Wistar Rats ◽  
Chinese Hamster ◽  
Cardiovascular Effects ◽  
Acute Effect ◽  
No Production ◽  
Acute Administration ◽  
Spontaneously Hypertensive ◽  
Vasorelaxant Effect ◽  
Beneficial Effects

Angiotensin-(1-7) (Ang-(1-7)) has been shown to have anti-hypertensive properties mediated through the receptor Mas . The beneficial effects of the Mas/Ang-(1-7) pathway prompted us to develop Ang-(1-7) analogues and peptides ligands for Mas. In the present study we evaluated the vasorelaxant and anti-hypertensive effect of the analogue A1317. To examine the NO production, chinese hamster ovary (CHO) cells transfected with Mas cDNA were incubated with A1317 at 10 -7 and 10 -6 mol/l for 60 minutes. Subsequently, the slices were mounted for evaluation by confocal microscopy. The vasorelaxant activity of the A1317 was measured in rings from Wistar rats and spontaneously hypertensive rats (SHR) descending thoracic aorta with functional endothelium pre-contracted with phenylephrine (0.1μM). To determine which receptor is involved in the vasorelaxant effect of the peptide experiment was performed in the presence of the Ang-(1-7) antagonist, A-779 (10 μm), in SHR rings. The acute effect of the peptide on arterial pressure was evaluated in male normotensive Wistar rats and SHR. Mean arterial pressure (MAP) and heart rate (HR) were monitored for 5 hours after in bolus administration of different doses of A1317 (0.1-12.5nmol/kg) in conscious animals. A1317 stimulated the NO production in CHO-Mas transfected cells and produced a concentration-dependent vasodilator effect in endothelium-containing aortic rings (Emax=18.97±1.33% in Wistar rings and 38.0±3.3% in SHR rings). The vasorelaxation produced by A1317 was attenuated by A779. Acute administration of A1317 reduced the MAP time and dose-dependently in conscious SHR. The reduction in MAP started to be significant after 130 minutes of the in bolus injection (Δ=-13±2.0mmHg; 0.5nmol/kg). The maximum change in MAP was observed after 4 hours of the in bolus injection (Δ=-21±4.0mmHg; 0.5nmol/kg). A1317 also produced a decrease in MAP of normotensive Wistar rats, however the magnitude of the MAP change was considerably smaller than that observed in SHR (Δ=-8.8±2.0mmHg). There was no significant effect of A1317 on HR of Wistar rats or SHR. These data suggest that the peptide A1317 presents antihypertensive and vasorelaxant properties and may have cardiovascular applications similar to those of Ang-(1-7).

scholarly journals Basic helix–loop–helix protein E47-mediated p21Waf1/Cip1 gene expression regulates apoptosis of intestinal epithelial cells

2007 ◽  
Vol 407 (2) ◽  
pp. 243-254 ◽  
Author(s):  
Sujoy Bhattacharya ◽  
Huazhang Guo ◽  
Ramesh M. Ray ◽  
Leonard R. Johnson
Keyword(s):  
Epithelial Cells ◽  
Caspase 3 ◽  
Intestinal Epithelial Cells ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Protein Levels ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Apoptotic Protein

Inhibition of ornithine decarboxylase by DFMO (α-difluromethylornithine) and subsequent polyamine depletion increases p21Cip1 protein, induces cell cycle arrest and confers resistance to apoptosis on intestinal epithelial cells. However, the mechanism by which polyamines regulate p21Cip1 expression and apoptosis is unknown. On the basis of the involvement of p21Cip1 as an anti-apoptotic protein, we tested the role of p21Cip1 in providing protection from apoptosis. Simultaneously, we investigated the role of E47, a basic helix–loop–helix protein, in the regulation of p21Cip1 gene transcription. Gene-specific siRNA (small interfering RNA) decreased E47 protein levels, increased p21Cip1 promoter activity and protein levels and protected cells from TNFα (tumour necrosis factor α)-induced apoptosis. Knockdown of p21Cip1 protein by siRNA resulted in cells becoming more susceptible to apoptosis. In contrast, incubation with EGF (epidermal growth factor) stimulated p21Cip1 mRNA and protein levels and rescued cells from apoptosis. During apoptosis, the level of E47 mRNA increased, causing a concomitant decrease in p21Cip1 mRNA and protein levels. Polyamine depletion decreased E47 mRNA levels and cell survival. Caspase 3-mediated cleavage of p130Cas has been implicated in p21Cip1 transcription. The progression of apoptosis led to a caspase 3-dependent cleavage of p130Cas and generated a 31 kDa fragment, which translocated to the nucleus, associated with nuclear E47 and inhibited p21Cip1 transcription. Polyamine depletion inhibited all these effects. Transient expression of the 31 kDa fragment prevented the expression of p21Cip1 protein and increased apoptosis. These results implicate p21Cip1 as an anti-apoptotic protein and suggest a role for polyamines in the regulation of p21Cip1 via the transcription repressor E47. Caspase-mediated cleavage of p130Cas generates a 31 kDa fragment, inhibits p21Cip1 transcription and acts as an amplifier of apoptotic signalling.

scholarly journals Impact of Different Physical Exercises on the Expression of Autophagy Markers in Mice

2021 ◽  
Vol 22 (5) ◽  
pp. 2635
Author(s):  
Ana P. Pinto ◽  
Alisson L. da Rocha ◽  
Bruno B. Marafon ◽  
Rafael L. Rovina ◽  
Vitor R. Muñoz ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Gastrocnemius Muscle ◽  
Acute Exercise ◽  
Colchicine Treatment ◽  
Heart Tissue ◽  
Beclin 1 ◽  
Liver Protein ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Exercise Induced

Although physical exercise-induced autophagy activation has been considered a therapeutic target to enhance tissue health and extend lifespan, the effects of different exercise models on autophagy in specific metabolic tissues are not completely understood. This descriptive investigation compared the acute effects of endurance (END), exhaustive (ET), strength (ST), and concurrent (CC) physical exercise protocols on markers of autophagy, genes, and proteins in the gastrocnemius muscle, heart, and liver of mice. The animals were euthanized immediately (0 h) and six hours (6 h) after the acute exercise for the measurement of glycogen levels, mRNA expression of Prkaa1, Ppargc1a, Mtor, Ulk1, Becn1, Atg5, Map1lc3b, Sqstm1, and protein levels of Beclin 1 and ATG5. The markers of autophagy were measured by quantifying the protein levels of LC3II and Sqstm1/p62 in response to three consecutive days of intraperitoneal injections of colchicine. In summary, for gastrocnemius muscle samples, the main alterations in mRNA expressions were observed after 6 h and for the ST group, and the markers of autophagy for the CC group were increased (i.e., LC3II and Sqstm1/p62). In the heart, the Beclin 1 and ATG5 levels were downregulated for the ET group. Regarding the markers of autophagy, the Sqstm1/p62 in the heart tissue was upregulated for the END and ST groups, highlighting the beneficial effects of these exercise models. The liver protein levels of ATG5 were downregulated for the ET group. After the colchicine treatment, the liver protein levels of Sqstm1/p62 were decreased for the END and ET groups compared to the CT, ST, and CC groups. These results could be related to diabetes and obesity development or liver dysfunction improvement, demanding further investigations.

Anti-IL-8 autoantibody:IL-8 immune complexes suppress spontaneous apoptosis of neutrophils

2007 ◽  
Vol 293 (2) ◽  
pp. L364-L374 ◽  
Author(s):  
Rafal Fudala ◽  
Agnieszka Krupa ◽  
Michael A. Matthay ◽  
Timothy C. Allen ◽  
Anna K. Kurdowska
Keyword(s):  
Immune Complexes ◽  
Caspase 3 ◽  
Morphological Changes ◽  
Human Neutrophils ◽  
Neutrophil Apoptosis ◽  
Spontaneous Apoptosis ◽  
Normal Human ◽  
Neutrophils Apoptosis ◽  
First Time

Our previous studies demonstrated that a significant fraction of interleukin-8 (IL-8) in lung fluids from patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) is associated with anti-IL-8 autoantibodies (anti-IL-8:IL-8 immune complexes). Neutrophils have been implicated in the pathogenesis of ALI/ARDS, and moreover, it is well-established that apoptosis of neutrophils is delayed in patients with ALI/ARDS. The aim of this study was, therefore, to examine the role of anti-IL-8:IL-8 immune complexes in modulating spontaneous apoptosis of normal human neutrophils. Apoptosis was assessed by evaluating morphological changes, measuring enzymatic activity of caspase-3, and determining the extent of DNA degradation. We found that samples containing anti-IL-8:IL-8 immune complexes but not samples from which these complexes were removed inhibited neutrophil apoptosis. Furthermore, the former samples or effectively anti-IL-8:IL-8 complexes induced an increase in the level of antiapoptotic protein, Bcl-XL. In contrast, levels of proapoptotic proteins Bax and Bak were decreased in the same conditions. Activity of both caspase-3 and caspase-9 was also suppressed by anti-IL-8:IL-8 complex-containing samples. Finally, we established that IgG receptor, FcγRIIa, mediates antiapoptotic activity of anti-IL-8:IL-8 complexes and that the key components of the FcγRIIa signaling pathway, Src, Syk, PI3 kinase, and ERK, may be involved in regulation of neutrophil apoptosis by the complexes. These studies demonstrate for the first time that anti-IL-8:IL-8 immune complexes have the ability to prolong neutrophil life.

Effect of leucine metabolite β-hydroxy-β-methylbutyrate on muscle metabolism during resistance-exercise training

1996 ◽  
Vol 81 (5) ◽  
pp. 2095-2104 ◽  
Author(s):  
S. Nissen ◽  
R. Sharp ◽  
M. Ray ◽  
J. A. Rathmacher ◽  
D. Rice ◽  
...  
Keyword(s):  
Exercise Training ◽  
Resistance Exercise ◽  
Muscle Metabolism ◽  
Linear Increase ◽  
Fat Free Mass ◽  
Resistance Exercise Training ◽  
Protein Levels ◽  
Linear Decrease ◽  
Exercise Induced ◽  
Leucine Metabolite

Nissen, S., R. Sharp, M. Ray, J. A. Rathmacher, D. Rice, J. C. Fuller, Jr., A. S. Connelly, and N. Abumrad. Effect of leucine metabolite β-hydroxy-β-methylbutyrate on muscle metabolism during resistance-exercise training. J. Appl. Physiol. 81(5): 2095–2104, 1996.—The effects of dietary supplementation with the leucine metabolite β-hydroxy-β-methylbutyrate (HMB) were studied in two experiments. In study 1, subjects ( n = 41) were randomized among three levels of HMB supplementation (0, 1.5 or 3.0 g HMB/day) and two protein levels (normal, 117 g/day, or high, 175 g/day) and weight lifted for 1.5 h 3 days/wk for 3 wk. In study 2, subjects ( n = 28) were fed either 0 or 3.0 g HMB/day and weight lifted for 2–3 h 6 days/wk for 7 wk. In study 1, HMB significantly decreased the exercise-induced rise in muscle proteolysis as measured by urine 3-methylhistidine during the first 2 wk of exercise (linear decrease, P < 0.04). Plasma creatine phosphokinase was also decreased with HMB supplementation ( week 3, linear decrease, P < 0.05). Weight lifted was increased by HMB supplementation when compared with the unsupplemented subjects during each week of the study (linear increase, P < 0.02). In study 2, fat-free mass was significantly increased in HMB-supplemented subjects compared with the unsupplemented group at 2 and 4–6 wk of the study ( P < 0.05). In conclusion, supplementation with either 1.5 or 3 g HMB/day can partly prevent exercise-induced proteolysis and/or muscle damage and result in larger gains in muscle function associated with resistance training.

Detrimental effect of combined exercise training and eNOS overexpression on cardiac function after myocardial infarction

2009 ◽  
Vol 296 (5) ◽  
pp. H1513-H1523 ◽  
Author(s):  
Monique C. de Waard ◽  
Jolanda van der Velden ◽  
Nicky M. Boontje ◽  
Dick H. W. Dekkers ◽  
Rien van Haperen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Exercise Training ◽  
Left Ventricular ◽  
Lv Function ◽  
Enos Expression ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Enos Uncoupling ◽  
Lv Remodeling ◽  
Exercise Induced

It has been reported that exercise after myocardial infarction (MI) attenuates left ventricular (LV) pump dysfunction by normalization of myofilament function. This benefit could be due to an exercise-induced upregulation of endothelial nitric oxide synthase (eNOS) expression and activity. Consequently, we first tested the hypothesis that the effects of exercise after MI can be mimicked by elevated eNOS expression using transgenic mice with overexpression of human eNOS (eNOSTg). Both exercise and eNOSTg attenuated LV remodeling and dysfunction after MI in mice and improved cardiomyocyte maximal force development (Fmax). However, only exercise training restored myofilament Ca2+-sensitivity and sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2a protein levels and improved the first derivative of LV pressure at 30 mmHg. Conversely, only eNOSTg improved survival. In view of these partly complementary actions, we subsequently tested the hypothesis that combining exercise and eNOSTg would provide additional protection against LV remodeling and dysfunction after MI. Unexpectedly, the combination of exercise and eNOSTg abolished the beneficial effects on LV remodeling and dysfunction of either treatment alone. The latter was likely due to perturbations in Ca2+ homeostasis, as myofilament Fmax actually increased despite marked reductions in the phosphorylation status of several myofilament proteins, whereas the exercise-induced increases in SERCA2a protein levels were lost in eNOSTg mice. Antioxidant treatment with N-acetylcysteine or supplementation of tetrahydrobiopterin and l-arginine prevented these detrimental effects on LV function while partly restoring the phosphorylation status of myofilament proteins and further enhancing myofilament Fmax. In conclusion, the combination of exercise and elevated eNOS expression abolished the cardioprotective effects of either treatment alone after MI, which appeared to be, at least in part, the result of increased oxidative stress secondary to eNOS “uncoupling.”

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