scholarly journals Acetylcholine Attenuates Hydrogen Peroxide-Induced Intracellular Calcium Dyshomeostasis Through Both Muscarinic and Nicotinic Receptors in Cardiomyocytes

2016 ◽  
Vol 39 (1) ◽  
pp. 341-349 ◽  
Author(s):  
Siripong Palee ◽  
Nattayaporn Apaijai ◽  
Krekwit Shinlapawittayatorn ◽  
Siriporn C. Chattipakorn ◽  
Nipon Chattipakorn
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Decay Rate ◽  
Acetylcholine Receptor ◽  
Nicotinic Receptors ◽  
Reactive Oxygen Species Generation ◽  
Receptor Blocker ◽  
Protective Effects ◽  
H2o2 Treatment ◽  
Muscarinic And Nicotinic Receptors

Background/Aims: Oxidative stress induced intracellular Ca2+ overload plays an important role in the pathophysiology of several heart diseases. Acetylcholine (ACh) has been shown to suppress reactive oxygen species generation during oxidative stress. However, there is little information regarding the effects of ACh on the intracellular Ca2+ regulation in the presence of oxidative stress. Therefore, we investigated the effects of ACh applied before or after hydrogen peroxide (H2O2) treatment on the intracellular Ca2+ regulation in isolated cardiomyocytes. Methods: Single ventricular myocytes were isolated from the male Wistar rats for the intracellular Ca2+ transient study by a fluorimetric ratio technique. Results: H2O2 significantly decreased both of intracellular Ca2+ transient amplitude and decay rate. ACh applied before, but not after, H2O2 treatment attenuated the reduction of intracellular Ca2+ transient amplitude and decay rate. Both atropine (a muscarinic acetylcholine receptor blocker) and mecamylamine (a nicotinic acetylcholine receptor blocker) significantly decreased the protective effects of acetylcholine on the intracellular Ca2+ regulation. Moreover, the combination of atropine and mecamylamine completely abolished the protective effects of acetylcholine on intracellular Ca2+ transient amplitude and decay rate. Conclusion: ACh pretreatment attenuates H2O2-induced intracellular Ca2+ dyshomeostasis through both muscarinic and nicotinic receptors.

scholarly journals Total Glucosides of Peony Protect Cardiomyocytes against Oxidative Stress and Inflammation by Reversing Mitochondrial Dynamics and Bioenergetics

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Mengmeng Wang ◽  
Qiang Li ◽  
Ying Zhang ◽  
Hao Liu
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lupus Erythematosus ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Bioenergetics ◽  
Protective Effects ◽  
Systemic Lupus ◽  
Regulatory Effects ◽  
Total Glucosides Of Peony

Total glucosides of peony (TGP) are used to treat rheumatoid arthritis and systemic lupus erythematosus. We explored the protective effects of TGP on cardiomyocyte oxidative stress and inflammation in the presence of hydrogen peroxide by focusing on mitochondrial dynamics and bioenergetics. Our study demonstrated that hydrogen peroxide significantly repressed cardiomyocyte viability and promoted cell apoptosis through induction of the mitochondrial death pathway. TGP treatment sustained cardiomyocyte viability, reduced cardiomyocyte apoptosis, and decreased inflammation and oxidative stress. Molecular investigation indicated that hydrogen peroxide caused mitochondrial dynamics disruption and bioenergetics reduction in cardiomyocytes, but this alteration could be normalized by TGP. We found that disruption of mitochondrial dynamics abolished the regulatory effects of TGP on mitochondrial bioenergetics; TGP modulated mitochondrial dynamics through the AMP-activated protein kinase (AMPK) pathway; and inhibition of AMPK alleviated the protective effects of TGP on mitochondria. Our results showed that TGP treatment reduces cardiomyocyte oxidative stress and inflammation in the presence of hydrogen peroxide by correcting mitochondrial dynamics and enhancing mitochondrial bioenergetics. Additionally, the regulatory effects of TGP on mitochondrial function seem to be mediated through the AMPK pathway. These findings are promising for myocardial injury in patients with rheumatoid arthritis and systemic lupus erythematosus.

scholarly journals Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide

2016 ◽  
Vol 17 (9) ◽  
pp. 692-702 ◽  
Author(s):  
Yun-zhi Ling ◽  
Xiao-hong Li ◽  
Li Yu ◽  
Ye Zhang ◽  
Qi-sheng Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effects ◽  
Primary Astrocytes

scholarly journals Protective effects of canolol against hydrogen peroxide-induced oxidative stress in AGS cells

RSC Advances ◽  
2017 ◽  
Vol 7 (68) ◽  
pp. 42826-42832 ◽  
Author(s):  
Ling Han ◽  
Xiaoyang Xia ◽  
Xia Xiang ◽  
Fenghong Huang ◽  
Zhen Zhang
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Phenolic Compound ◽  
Canola Oil ◽  
Protective Effects ◽  
Ags Cells

Canolol, a phenolic compound recently isolated from crude canola oil, effectively protected AGS cells against H2O2-induced oxidative stress.

scholarly journals Tamoxifen inhibits mitochondrial membrane damage caused by disulfiram

2017 ◽  
Vol 95 (5) ◽  
pp. 556-562 ◽  
Author(s):  
Natalia Pavón ◽  
Mabel Buelna-Chontal ◽  
Francisco Correa ◽  
Belem Yoval-Sánchez ◽  
Javier Belmont ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cytochrome C ◽  
Mitochondrial Membrane ◽  
Membrane Damage ◽  
Mitochondrial Swelling ◽  
Protective Effects ◽  
Mitochondrial Enzyme ◽  
Inner Membrane ◽  
Antioxidant Molecule

In this work, we studied the protective effects of tamoxifen (TAM) on disulfiram (Dis)-induced mitochondrial membrane insult. The results indicate that TAM circumvents the inner membrane leakiness manifested as Ca2+ release, mitochondrial swelling, and collapse of the transmembrane electric gradient. Furthermore, it was found that TAM prevents inactivation of the mitochondrial enzyme aconitase and detachment of cytochrome c from the inner membrane. Interestingly, TAM also inhibited Dis-promoted generation of hydrogen peroxide. Given that TAM is an antioxidant molecule, it is plausible that its protection may be due to the inhibition of Dis-induced oxidative stress.

Protective effects of catalpol against hydrogen peroxide induced oxidative stress on preimplantation porcine embryos

2014 ◽  
Vol 31 ◽  
pp. S214
Author(s):  
Deog-Bon Koo ◽  
Yong-Hee Lee ◽  
Sung-Hun Min ◽  
Jin-Woo Kim ◽  
Jae-Hyun Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effects
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