Exercise training reduces brainstem oxidative stress and restores normal breathing function in heart failure

Díaz, Hugo S.; Ríos-Gallardo, Angélica P.; Ortolani, Domiziana; Andrade, David C.; Toledo, Camilo; Pereyra, Katherin V.; Schwarz, Karla G.; Ramı́rez, Galo; Ortiz, Fernando C.; Andía, Marcelo E.; Río, Rodrigo R. del

doi:10.1016/j.freeradbiomed.2021.06.032

Cited by 10 publications

(18 citation statements)

References 43 publications

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“…PCR reactions were performed in a final volume of 10 µL using 1:10 diluted cDNA samples using the next thermal profile: initial enzyme activation by 3 min at 95 °C followed by 45 cycles consisting of: 3 s at 95 °C (denaturation) and 60 °C for 30 s (annealing/extension/acquisition), followed by a melting curve from 72 to 95 °C (0.3 °C/read). qPCR reactions were performed in duplicate for each sample, using the 2 ΔΔCT method for quantifications as described previously [ 44 , 45 ], using the geometric mean of CT values of control samples as internal calibrators for each target. We also tested the constitutive expression of 18S among all the experimental groups by using 2 −ΔCT comparisons between calibrator and treated samples ( Supplementary Table S2 ).…”

Section: Methodsmentioning

confidence: 99%

Lipid-Encapsuled Grape Tannins Prevent Oxidative-Stress-Induced Neuronal Cell Death, Intracellular ROS Accumulation and Inflammation

et al. 2022

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The central nervous system (CNS) is particularly vulnerable to oxidative stress and inflammation, which affect neuronal function and survival. Nowadays, there is great interest in the development of antioxidant and anti-inflammatory compounds extracted from natural products, as potential strategies to reduce the oxidative/inflammatory environment within the CNS and then preserve neuronal integrity and brain function. However, an important limitation of natural antioxidant formulations (mainly polyphenols) is their reduced in vivo bioavailability. The biological compatible delivery system containing polyphenols may serve as a novel compound for these antioxidant formulations. Accordingly, in the present study, we used liposomes as carriers for grape tannins, and we tested their ability to prevent neuronal oxidative stress and inflammation. Cultured catecholaminergic neurons (CAD) were used to establish the potential of lipid-encapsulated grape tannins (TLS) to prevent neuronal oxidative stress and inflammation following an oxidative insult. TLS rescued cell survival after H2O2 treatment (59.4 ± 8.8% vs. 90.4 ± 5.6% H2O2 vs. TLS+ H2O2; p < 0.05) and reduced intracellular ROS levels by ~38% (p < 0.05), despite displaying negligible antioxidant activity in solution. Additionally, TLS treatment dramatically reduced proinflammatory cytokines’ mRNA expression after H2O2 treatment (TNF-α: 400.3 ± 1.7 vs. 7.9 ± 1.9-fold; IL-1β: 423.4 ± 1.3 vs. 12.7 ± 2.6-fold; p < 0.05; H2O2 vs. TLS+ H2O2, respectively), without affecting pro/antioxidant biomarker expression, suggesting that liposomes efficiently delivered tannins inside neurons and promoted cell survival. In conclusion, we propose that lipid-encapsulated grape tannins could be an efficient tool to promote antioxidant/inflammatory cell defense.

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Section: Methodsmentioning

confidence: 99%

Lipid-Encapsuled Grape Tannins Prevent Oxidative-Stress-Induced Neuronal Cell Death, Intracellular ROS Accumulation and Inflammation

et al. 2022

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“…After vials each up-and-down turn, hold for 10 seconds for the flies to climb. Flies were exercised for 1.5 hours per day [32,33]. All exercise groups flies started exercise from when they were 2-day old, and underwent a 6day-long exercise program.…”

Section: Fly Stocks Diet and Husbandry And Exercise Training Protocolsmentioning

confidence: 99%

“…Exercise training improves the climbing performance in adult flies, and it delays age-related climbing performance decline in aging flies [37][38][39][40]. Increasing evidence confirmes that a 5-day EE reduces lipid accumulation in SM and HM, and it increases their antioxidant capacity in flies [28][29][30][31][32], but the molecular pathways through which EE regulates skeletal muscle lipid metabolism are poorly understood.…”

Section: Ee Prevented Sm From Damages Induced By a Hfd Or Mfsr In You...mentioning

confidence: 99%

“…Overexpression of Sirt1 also decreases the MAD level by enhancing antioxidant capacity in aged heart [25]. Finally, physical exercise reduces lipid accumulation in skeletal muscle and the heart, enhances their antioxidant capacity, and induces positive changes in FOXO, Sirt1 and PGC-1α (Peroxisome proliferator-activated receptorgamma coactivator) gene expression in muscle [28][29][30][31][32][33][34]. However, it remains unknown whether FOXO-specific expression in skeletal muscle and heart mediates exercise against defects induced by HFD in skeletal muscle and heart.…”

Section: Introductionmentioning

confidence: 99%

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Muscle FOXO-Specific Overexpression and Endurance Exercise Protect Skeletal Muscle and Heart from Defects Caused by a High-Fat Diet in Young Drosophila

Jin¹,

Wen²,

Hou³

2023

Front. Biosci. (Landmark Ed)

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Background: Obesity appears to significantly reduce physical activity, but it remains unclear whether this is related to obesity-induced damage to skeletal muscle (SM) and heart muscle (HM). Endurance exercise (EE) reduces obesity-induced defects in SM and HM, but its molecular mechanism is poorly understood. Methods: The UAS/GAL4 system was used to construct the regulation of SM-specific FOXO gene expression in Drosophila, and the transgenic drosophila was subjected to EE and high-fat diet (HFD) intervention. Results:The structure and function of SM and HM were impaired by a HFD and muscle-FOXO-specific RNAi (MFSR), including reduced climbing speed and climbing endurance, reduced fractional shortening of the heart, damaged myofibrils, and reduced mitochondria in HM. Besides, a HFD and MFSR increased triglyceride level and malondialdehyde level, decreased the Sirt1 and FOXO protein level, and reduced carnitine palmityl transferase I, superoxide dismutase, and catalase activity level, and they dow-regulated FOXO and bmm expression level in SM and HM. On the contrary, both muscle FOXO-specific overexpression (MFSO) and EE prevented abnormal changes of SM and HM in function, structure, or physiology caused by HFD and MFSR. Besides, EE also prevented defects of SM and HM induced by MFSR. Conclusions: Current findings confirmed MFSO and EE protected SM and heart from defects caused by a HFD via enhancing FOXO-realated antioxidant pathways and lipid catabolism. FOXO played a vital role in regulating HFD-induced defects in SM and HM, but FOXO was not a key regulatory gene of EE against damages in SM and HM. The mechanism was related to activity of Sirt1/FOXO/SOD (superoxide dismutase), CAT (catalase) pathways and lipid catabolism in SM and HM.

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“…Persistent/chronic neuroinflammation and oxidative stress create a complex positive feedback loop that induces and maintains elevated sympathetic activity in HFpEF mediated in part by central chemoreflex hypersensitivity. Indeed, high levels of reactive oxygen species (ROS) have been linked to sympatho-excitation in HF ( Díaz et al, 2020a ) and our lab has previously shown high levels of brainstem ROS in rats with HFpEF ( Díaz-Jara et al, 2021 ). In addition, recent studies from our lab in which we delivered brain-targeted pharmacological inhibition of ER stress restored normal cardiorespiratory function in HFpEF rats ( Díaz et al, 2021 ), suggesting an important link between neuroinflammation, oxidative stress, ER stress, and neuronal excitability in the brainstem.…”

Section: Introductionmentioning

confidence: 99%

Potential Role of the Retrotrapezoid Nucleus in Mediating Cardio-Respiratory Dysfunction in Heart Failure With Preserved Ejection Fraction

et al. 2022

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A strong association between chemoreflex hypersensitivity, disordered breathing, and elevated sympathetic activity has been shown in experimental and human heart failure (HF). The contribution of chemoreflex hypersensitivity in HF pathophysiology is incompletely understood. There is ample evidence that increased peripheral chemoreflex drive in HF with reduced ejection fraction (HFrEF; EF<40%) leads to pathophysiological changes in autonomic and cardio-respiratory control, but less is known about the neural mechanisms mediating cardio-respiratory disturbances in HF with preserved EF (HFpEF; EF>50%). Importantly, it has been shown that activation of the central chemoreflex worsens autonomic dysfunction in experimental HFpEF, an effect mediated in part by the activation of C1 catecholaminergic neurons neighboring the retrotrapezoid nucleus (RTN), an important region for central chemoreflex control of respiratory and autonomic function. Accordingly, the main purpose of this brief review is to discuss the possible role played by activation of central chemoreflex pathways on autonomic function and its potential role in precipitating disordered breathing in HFpEF. Improving understanding of the contribution of the central chemoreflex to the pathophysiology of HFpEF may help in development of novel interventions intended to improve cardio-respiratory outcomes in HFpEF.

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Exercise training reduces brainstem oxidative stress and restores normal breathing function in heart failure

Cited by 10 publications

References 43 publications

Lipid-Encapsuled Grape Tannins Prevent Oxidative-Stress-Induced Neuronal Cell Death, Intracellular ROS Accumulation and Inflammation

Lipid-Encapsuled Grape Tannins Prevent Oxidative-Stress-Induced Neuronal Cell Death, Intracellular ROS Accumulation and Inflammation

Muscle FOXO-Specific Overexpression and Endurance Exercise Protect Skeletal Muscle and Heart from Defects Caused by a High-Fat Diet in Young Drosophila

Potential Role of the Retrotrapezoid Nucleus in Mediating Cardio-Respiratory Dysfunction in Heart Failure With Preserved Ejection Fraction

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