Hypaconitine protects H9c2 cells from oxidative stress-induced apoptosis

2012 ◽  
Vol 6 (5) ◽  
Author(s):  
Zhi-Hui Li
Keyword(s):  
Oxidative Stress ◽  
H9c2 Cells ◽  
Induced Apoptosis

Cardioprotective effect of KR-33889, a novel PARP inhibitor, against oxidative stress-induced apoptosis in H9c2 cells and isolated rat hearts

2017 ◽  
Vol 40 (5) ◽  
pp. 640-654 ◽  
Author(s):  
Eun-Seok Park ◽  
Do-Hyun Kang ◽  
Jun Chul Kang ◽  
Yong Chang Jang ◽  
Min-Ju Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parp Inhibitor ◽  
Cardioprotective Effect ◽  
H9c2 Cells ◽  
Rat Hearts ◽  
Induced Apoptosis ◽  
Isolated Rat

Role of calreticulin in the sensitivity of myocardiac H9c2 cells to oxidative stress caused by hydrogen peroxide

2006 ◽  
Vol 290 (1) ◽  
pp. C208-C221 ◽  
Author(s):  
Yoshito Ihara ◽  
Yoshishige Urata ◽  
Shinji Goto ◽  
Takahito Kondo
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Molecular Chaperone ◽  
Vital Role ◽  
H9c2 Cells ◽  
Cardiac Physiology ◽  
Caspase 12 ◽  
A Cell ◽  
Induced Apoptosis

Calreticulin (CRT), a Ca2+-binding molecular chaperone in the endoplasmic reticulum, plays a vital role in cardiac physiology and pathology. Oxidative stress is a main cause of myocardiac apoptosis in the ischemic heart, but the function of CRT under oxidative stress is not fully understood. In the present study, the effect of overexpression of CRT on susceptibility to apoptosis under oxidative stress was examined using myocardiac H9c2 cells transfected with the CRT gene. Under oxidative stress due to H2O2, the CRT-overexpressing cells were highly susceptible to apoptosis compared with controls. In the overexpressing cells, the levels of cytoplasmic free Ca2+ ([Ca2+]i) were significantly increased by H2O2, whereas in controls, only a slight increase was observed. The H2O2-induced apoptosis was enhanced by the increase in [Ca2+]i caused by thapsigargin in control cells but was suppressed by BAPTA-AM, a cell-permeable Ca2+ chelator in the CRT-overexpressing cells, indicating the importance of the level of [Ca2+]i in the sensitivity to H2O2-induced apoptosis. Suppression of CRT by the introduction of the antisense cDNA of CRT enhanced cytoprotection against oxidative stress compared with controls. Furthermore, we found that the levels of activity of calpain and caspase-12 were elevated through the regulation of [Ca2+]i in the CRT-overexpressing cells treated with H2O2 compared with controls. Thus we conclude that the level of CRT regulates the sensitivity to apoptosis under oxidative stress due to H2O2 through a change in Ca2+ homeostasis and the regulation of the Ca2+-calpain-caspase-12 pathway in myocardiac cells.

scholarly journals Lingonberry anthocyanins protect cardiac cells from oxidative-stress-induced apoptosis

2017 ◽  
Vol 95 (8) ◽  
pp. 904-910 ◽  
Author(s):  
Cara K. Isaak ◽  
Jay C. Petkau ◽  
Heather Blewett ◽  
Karmin O ◽  
Yaw L. Siow
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Control Group ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Induced Apoptosis ◽  
Hoechst Staining

Lingonberry grown in northern Manitoba, Canada, contains exceptionally high levels of anthocyanins and other polyphenols. Previous studies from our lab have shown that lingonberry anthocyanins can protect H9c2 cells from ischemia–reperfusion injury and anthocyanin-rich diets have been shown to be associated with decreased cardiovascular disease and mortality. Oxidative stress can impair function and trigger apoptosis in cardiomyocytes. This study investigated the protective effects of physiologically relevant doses of lingonberry extracts and pure anthocyanins against hydrogen-peroxide-induced cell death. Apoptosis and necrosis were detected in H9c2 cells after hydrogen peroxide treatment via flow cytometry using FLICA 660 caspase 3/7 combined with YO-PRO-1 and then confirmed with Hoechst staining and fluorescence microscopy. Each of the 3 major anthocyanins found in lingonberry (cyanidin-3-galactoside, cyanidin-3-glucoside, and cyanidin-3-arabinoside) was protective against hydrogen-peroxide-induced apoptosis in H9c2 cells at 10 ng·mL−1 (20 nmol·L−1) and restored the number of viable cells to match the control group. A combination of the 3 anthocyanins was also protective and a lingonberry extract tested at 3 concentrations produced a dose-dependent protective effect. Lingonberry anthocyanins protected cardiac cells from oxidative-stress-induced apoptosis and may have cardioprotective effects as a dietary modification.

scholarly journals Discovering Antioxidant Molecules in the Archaea Domain: Peroxiredoxin Bcp1 fromSulfolobus solfataricusProtects H9c2 Cardiomyoblasts from Oxidative Stress

Archaea ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Carmen Sarcinelli ◽  
Gabriella Fiorentino ◽  
Elio Pizzo ◽  
Simonetta Bartolucci ◽  
Danila Limauro
Keyword(s):  
Oxidative Stress ◽  
Mammalian Cells ◽  
Sulfolobus Solfataricus ◽  
Thioredoxin Reductase ◽  
H9c2 Cells ◽  
H9c2 Cardiomyoblasts ◽  
Ph Conditions ◽  
Induced Apoptosis ◽  
Antioxidant Effects

Peroxiredoxins (Prxs) are ubiquitous thiol peroxidases that are involved in the reduction of peroxides. It has been reported that prokaryotic Prxs generally show greater structural robustness than their eukaryotic counterparts, making them less prone to inactivation by overoxidation. This difference has inspired the search for new antioxidants from prokaryotic sources that can be used as possible therapeutic biodrugs. Bacterioferritin comigratory proteins (Bcps) of the hyperthermophilic archaeonSulfolobus solfataricusthat belong to the Prx family have recently been characterized. One of these proteins, Bcp1, was chosen to determine its antioxidant effects in H9c2 rat cardiomyoblast cells. Bcp1 activity was measuredin vitrounder physiological temperature and pH conditions that are typical of mammalian cells; the yeast thioredoxin reductase (yTrxR)/thioredoxin (yTrx) reducing system was used to evaluate enzyme activity. A TAT-Bcp1 fusion protein was constructed to allow its internalization and verify the effect of Bcp1 on H9c2 rat cardiomyoblasts subjected to oxidative stress. The results reveal that TAT-Bcp1 is not cytotoxic and inhibits H2O2-induced apoptosis in H9c2 cells by reducing the H2O2content inside these cells.

scholarly journals Thrombopoietin Protects Cardiomyocytes from Iron-Overload Induced Oxidative Stress and Mitochondrial Injury

2015 ◽  
Vol 36 (5) ◽  
pp. 2063-2071 ◽  
Author(s):  
Shing Chan ◽  
Godfrey Chifung Chan ◽  
Jieyu Ye ◽  
Qizhou Lian ◽  
Jianliang Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Iron Overload ◽  
Protective Effect ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Lipid Hydroperoxides ◽  
Ros Production ◽  
H9c2 Cells ◽  
Induced Apoptosis

Background/Aims: Thalassaemia accompanied with iron-overload is common in Hong Kong. Iron-overload induced cardiomyopathy is the commonest cause of morbidity and mortality in patients with β-thalassaemia. Chronic iron-overload due to blood transfusion can cause cardiac failure. Decreased antioxidant defence and increased ROS production may lead to oxidative stress and cell injury. Iron-overload may lead to heart tissue damage through lipid peroxidation in response to oxidative stress, and a great diversity of toxic aldehydes are formed when lipid hydroperoxides break down in heart and plasma. Methods: Iron entry into embryonic heart H9C2 cells was determined by calcein assay using a fluorometer. Reactive oxygen species (ROS) production in cells treated with FeCl3 or thrombopoietin (TPO) was monitored by using the fluorescent probe H2DCFDA. Changes in mitochondrial membrane potential of H9C2 cells were quantified by using flow cytometry. Results: We demonstrated that iron induced oxidative stress and apoptosis in cardiomyocytes, and that iron increased ROS production and reduced cell viability in a dose-dependent manner. Iron treatment increased the proportion of cells with JC-1 monomers, indicating a trend of drop in the mitochondrial membrane potential. TPO exerted a cardio-protective effect on iron-induced apoptosis. Conclusions: These findings suggest that iron-overload leads to the generation of ROS and further induces apoptosis in cardiomyocytes via mitochondrial pathways. TPO might exert a protective effect on iron-overload induced apoptosis via inhibiting oxidative stress and suppressing the mitochondrial pathways in cardiomyocytes.

TPO exerts a protective effect on iron-overload induces apoptosis in cardiomyocytes via mitochondrial pathways

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4668-4668 ◽  
Author(s):  
Mo Yang ◽  
Shing Chan ◽  
Jie yu Ye ◽  
Godfrey ChiFung Chan
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Protective Effect ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Ros Production ◽  
H9c2 Cells ◽  
Plot Analysis ◽  
Iron Treatment ◽  
Induced Apoptosis

Thalassaemia companied with iron-overload is common in Hong Kong. Iron overload induced cardiomyopathy is the commonest cause of morbidity and mortality in b-thalassaemia patients. One of the causes of cardiac failure is chronic iron overload of blood transfusion. Some studies showed that iron overload can cause toxic effect in heart cells. Iron-overload induced cardiomyopathy damages are the major complications in patients with beta-thalassaemia major. Iron-overload may induce apoptosis in cardiomyocytes. Our previous study showed TPO has cardiac protective effect (Li et al, Circulation, 2007). In this study, we demonstrated firstly that iron induced oxidative stress can cause apoptosis in cardiomyocytes. By using H9C2 cells, we showed that iron increased reactive oxygen species (ROS) production (n=3) and reduced cell viability in a dose-dependent manner (0-0.6 mM) (n=6). Apoptotic cells were found to be significantly increased under iron treatment (0.3 mM, 72 hrs) in the AnnexinV/PI assay (n=6). The expression of active caspase-3 significantly increased in iron-treated cells. Furthermore, iron treatment increased the proportion of cells containing JC-1 monomers, indicating a trend in the drop of mitochondrial membrane potential (n=6). Secondly, we found that TPO exerted cardio-protective effect on iron-induced apoptosis. H9C2 cells were cultured in the presence of iron (0.3 mM) with or without TPO (50 ng/mL). The ROS production was significantly decreased with the addition of TPO at 50 ng/mL (n=3). Dot-plot analysis of AnnexinV/PI staining demonstrated that TPO significantly reduced the population of apoptotic cells (n=6). Incubation with TPO also decreased the iron-induced caspase-3 expression (n=6). Flow cytometric dot-plot analysis also showed trends of amelioration of the increase in JC-1 monomers in the iron plus TPO group (n=6), indicating a trend in attenuation of the drop of mitochondrial membrane potential. Our findings suggest that iron-overload lead to generation of ROS which further induces apoptosis in cardiomyocytes via mitochondrial pathways and TPO might exert a protective effect on iron-overload induced apoptosis via inhibiting oxidative stress and mitochondrial pathway in cardiomyocytes. Disclosures: No relevant conflicts of interest to declare.

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