scholarly journals NOX Inhibition Improves β Adrenergic-Stimulated Contractility and Intracellular Calcium Handling in the Aged Heart

2018 ◽  
Author(s):  
Alvaro Valdés ◽  
Guillermo Barrios ◽  
Nikol Ponce ◽  
Raul A Dulce ◽  
Daniel R Gonzalez
Keyword(s):  
Oxidative Stress ◽  
Intracellular Calcium ◽  
Negative Impact ◽  
Calcium Handling ◽  
Isolated Cardiomyocytes ◽  
Beta Adrenergic ◽  
Dependent Effect ◽  
Isolated Hearts ◽  
Nox Inhibitors ◽  
Isolated Cardiac Myocytes

Cardiac aging is characterized by alterations in contractility and intracellular calcium ([Ca2+]i) homeostasis. It has been suggested that oxidative stress may be involved in this process. We and others have reported that in cardiomyopathies the NADPH oxidase (NOX)-derived superoxide is increased, with a negative impact on [Ca2+]i and contractility. We tested the hypothesis that in the aged heart, [Ca2+]i handling and contractility are disturbed by NOX-derived superoxide. Contractility was evaluated isolated hearts, challenged with isoproterenol. To assess [Ca2+]i, isolated cardiac myocytes were field-stimulated and [Ca2+]i was monitored with fura-2. Cardiac concentration-response to isoproterenol was depressed in aged compared to adults hearts (p < 0.005), but was restored by NOX inhibitors apocynin and VAS2870. In isolated cardiomyocytes, apocynin increased the amplitude of [Ca2+]i in aged myocytes (p < 0.05). Time-50 [Ca2+]i decay was increased in aged myocytes (p < 0.05) and reduced towards normal by NOX inhibition. In addition, we found that myofilaments Ca2+ sensitivity was reduced in aged myocytes (p < 0.05), and further reduced by apocynin. Finally SERCA levels but not phospholamban were reduced in aged hearts (p < 0.05). In conclusion, β-adrenergic‒induced contractility was depressed in aged hearts, and NOX inhibition restored back to normal. Moreover, altered Ca2+ handling in aged myocytes was also improved by NOX inhibition. These results suggest a NOX-dependent effect in aged myocytes at the level of Ca2+ handling proteins and myofilaments.

scholarly journals NOX Inhibition Improves β-Adrenergic Stimulated Contractility and Intracellular Calcium Handling in the Aged Rat Heart

2018 ◽  
Vol 19 (8) ◽  
pp. 2404 ◽  
Author(s):  
Álvaro Valdés ◽  
Adriana Treuer ◽  
Guillermo Barrios ◽  
Nikol Ponce ◽  
Roberto Fuentealba ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Intracellular Calcium ◽  
Negative Impact ◽  
Calcium Handling ◽  
Isolated Cardiomyocytes ◽  
Isolated Hearts ◽  
Nox Inhibitors ◽  
Isolated Cardiac Myocytes ◽  
Old Rats ◽  
Phospholamban Phosphorylation

Cardiac aging is characterized by alterations in contractility and intracellular calcium ([Ca2+]i) homeostasis. It has been suggested that oxidative stress may be involved in this process. We and others have reported that in cardiomyopathies the NADPH oxidase (NOX)-derived superoxide is increased, with a negative impact on [Ca2+]i and contractility. We tested the hypothesis that in the aged heart, [Ca2+]i handling and contractility are disturbed by NOX-derived superoxide. For this we used adults (≈5 month-old) and aged (20–24 month-old) rats. Contractility was evaluated in isolated hearts, challenged with isoproterenol. To assess [Ca2+]i, isolated cardiac myocytes were field-stimulated and [Ca2+]i was monitored with fura-2. Cardiac concentration-response to isoproterenol was depressed in aged compared to adults hearts (p < 0.005), but was restored by NOX inhibitors apocynin and VAS2870. In isolated cardiomyocytes, apocynin increased the amplitude of [Ca2+]i in aged myocytes (p < 0.05). Time-50 [Ca2+]i decay was increased in aged myocytes (p < 0.05) and reduced towards normal by NOX inhibition. In addition, we found that myofilaments Ca2+ sensitivity was reduced in aged myocytes (p < 0.05), and was further reduced by apocynin. NOX2 expression along with NADPH oxidase activity was increased in aged hearts. Phospholamban phosphorylation (Ser16/Thr17) after isoproterenol treatment was reduced in aged hearts compared to adults and was restored by apocynin treatment (p < 0.05). In conclusion, β-adrenergic-induced contractility was depressed in aged hearts, and NOX inhibition restored back to normal. Moreover, altered Ca2+ handling in aged myocytes was also improved by NOX inhibition. These results suggest a NOX-dependent effect in aged myocytes at the level of Ca2+ handling proteins and myofilaments.

scholarly journals Liraglutide Preserves Intracellular Calcium Handling in Isolated Murine Myocytes Exposed to Oxidative Stress

2017 ◽  
pp. 889-895 ◽  
Author(s):  
S. PALEE ◽  
S. C. CHATTIPAKORN ◽  
N. CHATTIPAKORN
Keyword(s):  
Oxidative Stress ◽  
Decay Rate ◽  
Intracellular Calcium ◽  
Wistar Rats ◽  
Calcium Handling ◽  
Isolated Cardiomyocytes ◽  
Before And After ◽  
Male Wistar Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

In ischemic/reperfusion (I/R) injured hearts, severe oxidative stress occurs and is associated with intracellular calcium (Ca2+) overload. Glucagon-Like Peptide-1 (GLP-1) analogues have been shown to exert cardioprotection in I/R heart. However, there is little information regarding the effects of GLP-1 analogue on the intracellular Ca2+ regulation in the presence of oxidative stress. Therefore, we investigated the effects of GLP-1 analogue, (liraglutide, 10 µM) applied before or after hydrogen peroxide (H2O2, 50 µM) treatment on intracellular Ca2+ regulation in isolated cardiomyocytes. We hypothesized that liraglutide can attenuate intracellular Ca2+ overload in cardiomyocytes under H2O2-induced cardiomyocyte injury. Cardiomyocytes were isolated from the hearts of male Wistar rats. Isolated cardiomyocytes were loaded with Fura-2/AM and fluorescence intensity was recorded. Intracellular Ca2+ transient decay rate, intracellular Ca2+ transient amplitude and intracellular diastolic Ca2+ levels were recorded before and after treatment with liraglutide. In H2O2 induced severe oxidative stressed cardiomyocytes (which mimic cardiac I/R) injury, liraglutide given prior to or after H2O2 administration effectively increased both intracellular Ca2+ transient amplitude and intracellular Ca2+ transient decay rate, without altering the intracellular diastolic Ca2+ level. Liraglutide attenuated intracellular Ca2+ overload in H2O2-induced cardiomyocyte injury and may be responsible for cardioprotection during cardiac I/R injury by preserving physiological levels of calcium handling during the systolic and diastolic phases of myocyte activation.

Correlation between oxidative Stress and Alteration of Intracellular Calcium Handling in Isoproterenol-Induced Myocardial Infarction

2006 ◽  
Vol 289 (1-2) ◽  
pp. 125-136 ◽  
Author(s):  
Mauricio Díaz-Muñoz ◽  
Marco Antonio Álvarez-Pérez ◽  
Lucía Yáñez ◽  
Susana Vidrio ◽  
Lidia Martínez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Intracellular Calcium ◽  
Calcium Handling

Reduction of doxorubicin-induced cytotoxicity and mitochondrial damage by betanin in rat isolated cardiomyocytes and mitochondria

2021 ◽  
pp. 096032712110228
Author(s):  
AA Hafez ◽  
Z Jamali ◽  
S Samiei ◽  
S Khezri ◽  
A Salimi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Bioactive Compound ◽  
Isolated Cardiomyocytes ◽  
Cardiac Inflammation ◽  
Flow Cytometric ◽  
Significant Toxicity ◽  
Ros Formation ◽  
Gene Regulatory ◽  
And Oxidative Stress

Doxorubicin (DOX) is an anticancer drug which is used for treatment of several types of cancers. But the clinical use of doxorubicin is limited because of its cardiotoxicity and cardiomyopathy. Mitochondrial-dependent oxidative stress and cardiac inflammation appear to be involved in doxorubicin-induced cardiotoxicity. Betanin as a bioactive compound in Beetroot ( Beta vulgaris L.) displays anti-radical, antioxidant gene regulatory and cardioprotective activities. In this current study, we investigated the protective effect of betanin on doxorubicin-induced cytotoxicity and mitochondrial-dependent oxidative stress in isolated cardiomyocytes and mitochondria. Isolated cardiomyocytes and mitochondria were treated with three concentrations of betanin (1, 5 and 10 µM) and doxorubicin (3.5 µM) for 6 h. The parameters of cellular and mitochondrial toxicity were analyzed using biochemical and flow cytometric methods. Our results showed a significant toxicity in isolated cardiomyocytes and mitochondria in presence of doxorubicin which was related to reactive oxygen species (ROS) formation, increase in malondialdehyde (MDA), increase in oxidation of GSH to GSSG, lysosomal/mitochondrial damages and mitochondrial swelling. While betanin pretreatment reverted doxorubicin-induced cytotoxicity and oxidative stress in isolated cardiomyocytes and mitochondria. These results suggest that betanin elicited a typical protective effect on doxorubicin-induced cytotoxicity and oxidative stress. It is possible that betanin could be used as a useful adjuvant in combination with doxorubicin chemotherapy for reduction of cardiotoxicity and cardiomyopathy.

Role of organic cation mediated transport and oxidative stress in the synephrine induced-toxicity in freshly isolated cardiomyocytes

2010 ◽  
Vol 196 ◽  
pp. S142
Author(s):  
L.G. Rossato ◽  
V.M. Costa ◽  
P.G. Pinho ◽  
F. Carvalho ◽  
H. Carmo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Organic Cation ◽  
Isolated Cardiomyocytes ◽  
And Oxidative Stress
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