Dietary restriction and fibre supplementation: oxidative stress and metabolic shifting for cardiac health

2003 ◽  
Vol 81 (11) ◽  
pp. 1042-1048 ◽  
Author(s):  
Yeda S Diniz ◽  
Antonio C Cicogna ◽  
Carlos R Padovani ◽  
Maeli D.P Silva ◽  
Luciane A Faine ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dietary Restriction ◽  
Dietary Fibre ◽  
Cardiac Tissue ◽  
Citrate Synthase ◽  
Lipid Hydroperoxide ◽  
Hdl Cholesterol ◽  
Main Process ◽  
Beneficial Effects ◽  
Male Wistar Rats

Dietary modification ought to be the first line of strategy in prevention of the development of cardiac disease. The purpose of this study was to investigate whether dietary restriction, dietary-fibre-enriched diet, and their interactions might affect antioxidant capacity and oxidative stress in cardiac tissue. Male Wistar rats (180–200 g; n = 10) were divided into four groups: control ad libitum diet (C), 50% restricted diet (DR), fed with fibre-enriched diet (F), and 50% restricted fibre-enriched diet (DR-F). After 35 days of the treatments, F, DR, and DR-F rats showed low cholesterol, LDL-cholesterol, and triacylglycerol, and high HDL-cholesterol in serum. The DR, DR-F, and F groups had decreased myocardial lipoperoxide and lipid hydroperoxide. The DR-F and F treatments increased superoxide dismutase and glutatione peroxidase (GSH-Px). The DR treatment increased GSH-Px and catalase activities. Dietary fibre beneficial effects were related to metabolic alterations. The F and DR-F groups showed high cardiac glycogen and low lactate dehydrogenase/citrate synthase ratios, indicating diminished anaerobic and elevated aerobic myocardial metabolism in these animals. There was no synergistic effect between dietary restriction and dietary fibre addition, since no differences were observed in markers of oxidative stress in the F and DR-F groups. Dietary fibre supplementation, rather than energy intake and dietary restriction, appears to be the main process retarding oxidative stress in cardiac tissue.Key words: dietary fibre, dietary restriction, cardiac tissue, oxidative stress.

scholarly journals Effects of Apocynin on Heart Muscle Oxidative Stress of Rats with Experimental Diabetes: Implications for Mitochondria

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 335
Author(s):  
Estefanía Bravo-Sánchez ◽  
Donovan Peña-Montes ◽  
Sarai Sánchez-Duarte ◽  
Alfredo Saavedra-Molina ◽  
Elizabeth Sánchez-Duarte ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Sensitivity ◽  
Cardiac Tissue ◽  
Diabetic Rats ◽  
Oxidase Inhibitor ◽  
Beneficial Effects ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Transport Chain ◽  
Male Wistar Rats

Diabetes mellitus (DM) constitutes one of the public health problems today. It is characterized by hyperglycemia through a defect in the β-cells function and/or decreased insulin sensitivity. Apocynin has been tasted acting directly as an NADPH oxidase inhibitor and reactive oxygen species (ROS) scavenger, exhibiting beneficial effects against diabetic complications. Hence, the present study’s goal was to dissect the possible mechanisms by which apocynin could mediate its cardioprotective effect against DM-induced oxidative stress. Male Wistar rats were assigned into 4 groups: Control (C), control + apocynin (C+A), diabetes (D), diabetes + apocynin (D+A). DM was induced with streptozotocin. Apocynin treatment (3 mg/kg/day) was applied for 5 weeks. Treatment significantly decreased blood glucose levels and insulin resistance in diabetic rats. In cardiac tissue, ROS levels were higher, and catalase enzyme activity was reduced in the D group compared to the C group; the apocynin treatment significantly attenuated these responses. In heart mitochondria, Complexes I and II of the electron transport chain (ETC) were significantly enhanced in the D+A group. Total glutathione, the level of reduced glutathione (GSH) and the GSH/ oxidized glutathione (GSSG) ratio were increased in the D+A group. Superoxide dismutase (SOD) and the glutathione peroxidase (GSH-Px) activities were without change. Apocynin enhances glucose uptake and insulin sensitivity, preserving the antioxidant defense and mitochondrial function.

Beneficial effects of linum usitatissimum L. on dyslipidemia, oxidative stress and inflammatory cytokines in hypercholesterolemic rats

2019 ◽  
Vol 49 (4) ◽  
pp. 777-790 ◽  
Author(s):  
Sarra Dali ◽  
Djamil Krouf ◽  
Zoheir Mellouk ◽  
Nawal Taleb-Dida
Keyword(s):  
Oxidative Stress ◽  
Linum Usitatissimum ◽  
Hdl Cholesterol ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Casein Diet ◽  
Content Type ◽  
Beneficial Effects ◽  
Linum Usitatissimum L ◽  
Male Wistar Rats

Purpose This paper aims to study the effects of a diet supplemented with flaxseeds on dyslipidemia, oxidative stress and proinflammatory cytokines, in rats consuming a high-cholesterol diet. Design/methodology/approach Male Wistar rats (n = 30) weighing (250 ± 5 g) of which 10 were control and 20 were rendered hypercholesterolemic (HC) by feeding a diet enriched with 1% of cholesterol, for 15 days. After this phase, rats were divided into two groups; hypercholesterolemic group (HC) (n = 10), fed 20% casein diet enriched with 1% cholesterol; and hypercholesterolemic rats fed the same diet (n = 10), but additionally supplemented with flaxseeds (Linum usitatissimum) (Lu) powder, i.e. HC-Lu. Animals of the control group (n = 10) were fed the casein diet. All the animals were maintained on the respective diets for four weeks. Findings This study showed that in HC-Lu as compared to HC group, plasma total cholesterol, triacylglycerols and non-HDL cholesterol concentrations were respectively 2.4-, 1.5- and 3-fold lower. Also, the lipid peroxidation was reduced in red blood cells, organs (liver, heart and aorta) and lipoproteins (HDL2, HDL3 and VDL-LDL). A higher superoxide dismutase activity was observed in liver (+61%), heart (+62%) and aorta (+59%), whereas plasma proinflammatory cytokine (IL-1beta and IL-6) levels were decreased. Originality/value These results suggest that flaxseeds help to reduce hypercholesterolemia, oxidative stress and inflammation in patients with hypercholesterolemia.

scholarly journals Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats

2017 ◽  
Vol 43 (4) ◽  
pp. 1449-1459 ◽  
Author(s):  
Renata A. C. Silva ◽  
Andréa F. Gonçalves ◽  
Priscila P. dos Santos ◽  
Bruna Rafacho ◽  
Renan F. T. Claro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinoic Acid ◽  
Energy Metabolism ◽  
Cardiac Remodeling ◽  
Citrate Synthase ◽  
Isolated Heart ◽  
Lipid Hydroperoxide ◽  
Dependent Manner ◽  
Heart Study ◽  
Dose Dependent

Background/Aims: This study aimed to discern whether the cardiac alterations caused by retinoic acid (RA) in normal adult rats are physiologic or pathologic. Methods and Results: Wistar rats were assigned into four groups: control animals (C, n = 20) received a standard rat chow; animals fed a diet supplemented with 0.3 mg/kg/day all-trans-RA (AR1, n = 20); animals fed a diet supplemented with 5 mg/kg/day all-trans-RA (AR2, n = 20); and animals fed a diet supplemented with 10 mg/kg/day all-trans-RA (AR3, n = 20). After 2 months, the animals were submitted to echocardiogram, isolated heart study, histology, energy metabolism status, oxidative stress condition, and the signaling pathway involved in the cardiac remodeling induced by RA. RA increased myocyte cross-sectional area in a dose-dependent manner. The treatment did not change the morphological and functional variables, assessed by echocardiogram and isolated heart study. In contrast, RA changed catalases, superoxide dismutase, and glutathione peroxidases and was associated with increased values of lipid hydroperoxide, suggesting oxidative stress. RA also reduced citrate synthase, enzymatic mitochondrial complex II, ATP synthase, and enzymes of fatty acid metabolism and was associated with increased enzymes involved in glucose use. In addition, RA increased JNK 1/2 expression, without changes in TGF-β, PI3K, AKT, NFκB, S6K, and ERK. Conclusion: In normal rats, RA induces cardiac hypertrophy in a dose-dependent manner. The non-participation of the PI3K/Akt pathway, associated with the participation of the JNK pathway, oxidative stress, and changes in energy metabolism, suggests that cardiac remodeling induced by RA supplementation is deleterious.

scholarly journals Isosteviol ameliorates diabetic cardiomyopathy in rats by inhibiting ERK and NF-κB signaling pathways

2018 ◽  
Vol 238 (1) ◽  
pp. 47-60 ◽  
Author(s):  
Sheng-Gao Tang ◽  
Xiao-Yu Liu ◽  
Ji-Ming Ye ◽  
Ting-Ting Hu ◽  
Ying-Ying Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Diabetic Cardiomyopathy ◽  
Nuclear Factor Κb ◽  
Diabetic Rats ◽  
Signal Pathways ◽  
Mortality And Morbidity ◽  
Beneficial Effects ◽  
Male Wistar Rats ◽  
Glucose Plasma

Diabetes-induced injury of myocardium, defined as diabetic cardiomyopathy (DCM), accounts for significant mortality and morbidity in diabetic population. Alleviation of DCM by a potent drug remains considerable interests in experimental and clinical researches because hypoglycemic drugs cannot effectively control this condition. Here, we explored the beneficial effects of isosteviol sodium (STVNa) on type 1 diabetes-induced DCM and the potential mechanisms involved. Male Wistar rats were induced to diabetes by injection of streptozotocin (STZ). One week later, diabetic rats were randomly grouped to receive STVNa (STZ/STVNa) or its vehicle (STZ). After 11 weeks of treatment or 11 weeks treatment following 4 weeks of removal of the treatment, the cardiac function and structure were evaluated and related mechanisms were investigated. In diabetic rats, oxidative stress, inflammation, blood glucose and plasma advanced glycation end products (AGEs) were significantly increased, whereas superoxide dismutase 2 (SOD-2) expression and activity were decreased. STVNa treatment inhibited cardiac hypertrophy, fibrosis and inflammation, showed similar ratio of heart to body weight and antioxidant capacities almost similar to the normal controls, which can be sustained at least 4 weeks. Moreover, STVNa inhibited diabetes-inducted stimulation of both extracellular signal-regulated kinase (ERK) and nuclear factor κB (NF-κB) signal pathways. However, blood glucose, plasma AGE and insulin levels were not altered by STVNa treatment. These results indicate that STVNa may be developed into a potent therapy for DCM. The mechanism underlying this therapeutic effect involves the suppression of oxidative stress and inflammation by inhibiting ERK and NF-κB without changing blood glucose or AGEs.

scholarly journals Lipid profile, apolipoprotein A-I and oxidative stress in professional footballers, sedentary individuals, and their relatives

2011 ◽  
Vol 55 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Aline Margioti Zanella ◽  
Marcelo Arruda Nakazone ◽  
Marcela Augusta Souza Pinhel ◽  
Dorotéia Rossi Silva Souza
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Physical Exercise ◽  
Lipid Profile ◽  
Ldl Cholesterol ◽  
Hdl Cholesterol ◽  
Beneficial Effects ◽  
Apolipoprotein A ◽  
And Oxidative Stress ◽  
Cholesterol Fraction

OBJECTIVE: To evaluate whether lipid profile (LP), apolipoprotein A-1 (apo A-I) and malondialdehyde (MDA) have any relationship with physical exercise by comparing the groups of footballers (FG) with sedentary individuals (CG) and their relatives (RFG and RCG). SUBJECTS AND METHODS: Twenty individuals from FG and CG, 60 from RFG, and 57 from RCG were studied. RESULTS: FG showed lower levels of total cholesterol (119.5 ± 37.9 mg/dL), LDL-cholesterol fraction (53.6 ± 30.3), apo A-I (116.7 ± 11.9), and higher level of HDL-cholesterol fraction (HDLc) (49.7 ± 8.5) compared to RFG (148.3 ± 36.9, P = 0.02; 82.4 ± 37.7, P < 0.01; 124.6 ± 10.2, P = 0.03; and 42.7 ± 7.7, P < 0.01; respectively). Moreover, FG had reduced levels of MDA (101.0 ± 77.0 ng/mL) compared to CG (290.0 ± 341.0, P = 0.03) and RFG (209.9 ± 197.5, P = 0.04). CONCLUSIONS: These results suggest an association between physical exercise and lower levels of MDA in FG. Physical activity seems to promote beneficial effects on the LP regardless of the genetic influence considering HDLc levels.

scholarly journals Melatonin Reduces Oxidative Stress in the Right Ventricle of Newborn Sheep Gestated under Chronic Hypoxia

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1658
Author(s):  
Alejandro Gonzaléz-Candia ◽  
Pamela V. Arias ◽  
Simón A. Aguilar ◽  
Esteban G. Figueroa ◽  
Roberto V. Reyes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Right Ventricle ◽  
Manganese Superoxide Dismutase ◽  
Cardiac Tissue ◽  
Chronic Hypoxia ◽  
Experimental Period ◽  
Health Concern ◽  
Right Ventricle Dysfunction ◽  
Beneficial Effects ◽  
Pulmonary Arterial

Pulmonary arterial hypertension of newborns (PAHN) constitutes a critical condition involving both severe cardiac remodeling and right ventricle dysfunction. One main cause of this condition is perinatal hypoxia and oxidative stress. Thus, it is a public health concern for populations living above 2500 m and in cases of intrauterine chronic hypoxia in lowlands. Still, pulmonary and cardiac impairments in PAHN lack effective treatments. Previously we have shown the beneficial effects of neonatal melatonin treatment on pulmonary circulation. However, the cardiac effects of this treatment are unknown. In this study, we assessed whether melatonin improves cardiac function and modulates right ventricle (RV) oxidative stress. Ten lambs were gestated, born, and raised at 3600 m. Lambs were divided in two groups. One received daily vehicle as control, and another received daily melatonin (1 mg·kg−1·d−1) for 21 days. Daily cardiovascular measurements were recorded and, at 29 days old, cardiac tissue was collected. Melatonin decreased pulmonary arterial pressure at the end of the experimental period. In addition, melatonin enhanced manganese superoxide dismutase and catalase (CAT) expression, while increasing CAT activity in RV. This was associated with a decrease in superoxide anion generation at the mitochondria and NADPH oxidases in RV. Finally, these effects were associated with a marked decrease of oxidative stress markers in RV. These findings support the cardioprotective effects of an oral administration of melatonin in newborns that suffer from developmental chronic hypoxia.

scholarly journals A Role for Both V1a and V2 Receptors in Renal Heat Stress Injury Amplified by Rehydration with Fructose

2019 ◽  
Vol 20 (22) ◽  
pp. 5764
Author(s):  
Fernando E. García-Arroyo ◽  
Itzel Muñoz-Jiménez ◽  
Guillermo Gonzaga ◽  
Edilia Tapia ◽  
Horacio Osorio-Alonso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Renal Damage ◽  
Tap Water ◽  
Renin Angiotensin System ◽  
Stress Injury ◽  
Mild Heat ◽  
Beneficial Effects ◽  
Vasopressin Receptors ◽  
Male Wistar Rats

Chronic vasopressin secretion induced by recurrent mild heat stress exposure is significantly enhanced by limited rehydration with a fructose-containing beverage both in rodents and in humans. Moreover, this effect has been associated with upregulation of the polyol–fructokinase pathway and increased renal oxidative stress. Previously, we have shown that pharmacological inhibition of both V1a and V2 vasopressin receptors with conivaptan improved such renal alterations. The aim of this study was to evaluate the independent contributions of V1a and V2 receptors to the renal damage caused by mild heat stress and limited rehydration with a fructose-containing beverage. Osmotic minipumps were used to deliver either relcovaptan (0.64 mg/day) or tolvaptan (0.25 mg/day) in male Wistar rats for two weeks. Corresponding dilution vehicles were used as controls. To induce dehydration, rats were exposed to mild heat stress (37 °C for 1 h, Monday to Friday). All groups received a 10% fructose solution as a rehydration fluid for 2 h after mild heat stress. For the remainder of the day and on weekends, rats received tap water. The independent blockade of either the V1a or the V2 receptor prevented renal damage, reduced oxidative stress, and decreased plasma cortisol and systemic inflammation. However, the beneficial effects were regulated by different mechanisms. Tolvaptan inhibited polyol–fructokinase pathway overactivation, while relcovaptan prevented upregulation of the renin–angiotensin system and SGK1 expression. These data suggest that both V1a and V2 receptors participate in renal damage caused by heat stress-induced dehydration when fructose-containing beverages are used as rehydration fluids.

scholarly journals Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

2013 ◽  
Vol 64 (4) ◽  
pp. 521-529 ◽  
Author(s):  
Olusegun Kayode Afolabi ◽  
Emmanuel Bukoye Oyewo ◽  
Adeniran Sanmi Adekunle ◽  
Olaniyi Tope Adedosu ◽  
Adebayo Lawrence Adedeji
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Plasma Cholesterol ◽  
Interleukin 2 ◽  
Lipid Hydroperoxide ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Pon1 Activity ◽  
Pro Inflammatory Cytokines

Abstract The aim of this study was to establish the effects of fluoride on lipid metabolism and attendant inflammatory response by exposing rats to 50 mg L-1 and 100 mg L-1 of fluoride through drinking water for seven weeks. Both concentrations led to hypercholesterolemia while the 100 mg L-1 concentration induced hypertriglyceridaemia. High density lipoprotein (HDL) cholesterol levels dropped in the exposed rats while interleukin 2 (IL-2) increased more than 1.5-fold (p<0.05) and IL-6 and plasma TNF-α more than 2.5 fold (p<0.05). Fluoride-exposed rats also had significantly higher levels of liver malondialdehyde (MDA) and plasma lipid hydroperoxide (LOOH) but lower plasma paraoxonase (PON1) activity. Oxidative stress indices correlated with pro-inflammatory cytokines and plasma cholesterol. In contrast, proinflammatory cytokines inversely correlated with plasma triglyceride, HDL cholesterol and PON1. Our results suggest that the association between fluoride exposure with cardiovascular diseases may be related to its ability to disturb lipid homeostasis, and trigger pro-inflammatory cytokines and oxidative stress.

scholarly journals EXPRESSION OF APELIN IS RELATED TO OXIDATIVE DAMAGE IN HEART TISSUE OF RATS DURING CHRONIC SYSTEMIC HYPOXIA

2019 ◽  
Vol 1 (2) ◽  
pp. 68-75
Author(s):  
H R Helmi ◽  
Frans Ferdinal ◽  
Ani Retno Prijanti ◽  
Sri Widia A Jusman ◽  
Frans D Suyatna
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Heart Tissue ◽  
Male Rats ◽  
Heart Weight ◽  
Control Group ◽  
Sprague Dawley ◽  
Relative Expression ◽  
Beneficial Effects ◽  
Systemic Hypoxia

Background: Chronic systemic hypoxia is severe environmental stress for the heart and might lead to the development of heart failure. Apelin is an endogenous peptide that has been shown to have various beneficial effects on cardiac function. Apelin appears to have a role to play in the ventricular dysfunction and maintaining the performance of the heart.Objectives: In the present study we want to investigate the adaptive response of heart tissue to chronic systemic hypoxia and the correlation with apelin expression and oxidative stress in rat. Methods: An experimental study was performed using 28 Sprague-Dawley male rats, 8 weeks of age. Rats were divided into 7 groups 4 each, namely control group; normoxia (O2 atmosphere) and the treatment group of hypoxia (8% O2) for 6 hours; 1;3;5;7 and 14 days respectively. Body weight and heart weight were measured at each treatment. Ventricular thickness was measured by caliper, Apelin mRNA was measured using real-time qRT-PCR with Livak formula and malondialdehyde (MDA) level was used to assess oxidative stress due to cardiac tissue hypoxia.Results: Macroscopic exams showed hypertrophy at day 7th. The relative expression of Apelin mRNA in hypoxic heart is decreased at the beginning and then increased, starting from day-7 to day-14. The MDA levels were significantly increased from day-7 and were strongly correlated with relative expression Apelin.Conclusion:  It is concluded that the increase of Apelin expression is related to oxidative stress in heart tissue of rats during chronic systemic hypoxia.

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