scholarly journals Heart Failure and Stress Response

2015 ◽  
Vol 1 (3) ◽  
pp. 33-35
Author(s):  
Alessandro Pingitore ◽  
Francesca Mastorci ◽  
Giorgio Iervasi
2009 ◽  
Vol 126 (6) ◽  
pp. 779-789 ◽  
Author(s):  
Santiago Reyes ◽  
Sungjo Park ◽  
Bruce D. Johnson ◽  
Andre Terzic ◽  
Timothy M. Olson

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Xiang Wang ◽  
Tongjuan Tang ◽  
Mengting Zhai ◽  
Ruirui Ge ◽  
Liang Wang ◽  
...  

Objectives. Ling-Gui-Zhu-Gan decoction (LGZGD) is a potentially effective treatment for heart failure, and it showed significant anti-inflammatory potential in our previous studies. However, its ability to ameliorate heart failure through regulation of oxidative stress response is still unknown. This study was aimed to investigate the protective effect of LGZGD-containing serum on H2O2-induced oxidative injury in H9c2 cells and explore the underlying mechanism. Methods. Eighteen rats were randomly divided into two groups: the blank control group and LGZGD group. The LGZGD group rats were administrated with 8.4 g/kg/d LGZGD for seven consecutive days through gavage, while the blank control group rats were given an equal volume of saline. The serum was extracted from all the rats. To investigate the efficacy and the underlying mechanism of LGZGD, we categorized the H9c2 cells into groups: the control group, model group, normal serum control (NSC) group, LGZGD group, LGZGD + all-trans-retinoic acid (ATRA) group, and ATRA group. Malonedialdehyde (MDA) and superoxide dismutase (SOD) were used as markers for oxidative stress. Dichlorodihydrofluorescin diacetate (DCFH-DA) staining was used to measure the levels of reactive oxygen species (ROS). The apoptosis rate was detected using flow cytometry. The expression levels of pro-caspase-3, cleaved-caspase-3, Bcl-2, Bax, Keap1, Nrf2, and HO-1 were measured using western blotting. The mRNA levels of Keap1, Nrf2, and HO-1 were measured using RT-qPCR. Results. The LGZGD attenuated injury to H9c2 cells and reduced the apoptosis rate. It was also found to upregulate the SOD activity and suppress the formation of MDA and ROS. The expression levels of pro-caspase-3 and Bcl-2 were significantly increased, while those of cleaved-caspase-3 and Bax were decreased in the LGZGD group compared with the model group. As compared with the model group, the LGZGD group demonstrated decreased Keap1 protein expression and significantly increased Nrf2 nuclear expression and Nrf2-mediated transcriptional activity. ATRA was found to reverse the LGZGD-mediated antioxidative and antiapoptotic effect on injured H9c2 cells induced by H2O2. Conclusion. Our results demonstrated that LGZGD attenuated the H2O2-induced injury to H9c2 cells by inhibiting oxidative stress and apoptosis via the Nrf2/Keap1/HO-1 pathway. These observations suggest that LGZGD might prevent and treat heart failure through regulation of the oxidative stress response.


2013 ◽  
Vol 453 (3) ◽  
pp. 321-336 ◽  
Author(s):  
Darius J. R. Lane ◽  
Michael Li-Hsuan Huang ◽  
Samantha Ting ◽  
Sutharshani Sivagurunathan ◽  
Des R. Richardson

FRDA (Friedreich's ataxia) is a debilitating mitochondrial disorder leading to neural and cardiac degeneration, which is caused by a mutation in the frataxin gene that leads to decreased frataxin expression. The most common cause of death in FRDA patients is heart failure, although it is not known how the deficiency in frataxin potentiates the observed cardiomyopathy. The major proposed biochemical mechanisms for disease pathogenesis and the origins of heart failure in FRDA involve metabolic perturbations caused by decreased frataxin expression. Additionally, recent data suggest that low frataxin expression in heart muscle of conditional frataxin knockout mice activates an integrated stress response that contributes to and/or exacerbates cardiac hypertrophy and the loss of cardiomyocytes. The elucidation of these potential mechanisms will lead to a more comprehensive understanding of the pathogenesis of FRDA, and will contribute to the development of better treatments and therapeutics.


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Li-Xia Lou ◽  
Ai-Ming Wu ◽  
Dong-Mei Zhang ◽  
Sheng-Xian Wu ◽  
Yong-Hong Gao ◽  
...  

Objective. To explore the mechanism of cardioprotective effects of Chinese medicine, Yiqi Huoxue recipe, in rats with myocardial infarction- (MI-) induced heart failure.Methods. Male Sprague-Dawley rats underwent left anterior descending artery (LAD) ligation or sham operation. The surviving MI rats were divided randomly into three groups: MI (5 mL/kg/d NS by gavage), MI + Metoprolol Tartrate (MT) (12 mg/kg/d MT by gavage), and MI + Yiqi Huoxue (5 mL/kg recipe by gavage). And the sham operation rats were given 5 mL/kg/d normal saline. Treatments were given on the day following surgery for 4 weeks. Then rats were detected for heart structure and function by transthoracic echocardiography. Apoptosis in heart tissues was detected by TUNEL staining. To determine whether the endoplasmic reticulum (ER) stress response pathway is included in the cardioprotective function of the recipe, ER stress related proteins such as GRP78 and caspase-12 were examined.Results. Yiqi Huoxue recipe attenuated heart function injury, reversed histopathological damage, alleviated myocardial apoptosis and inhibited ER stress in MI rats.Conclusion. All the results suggest that Yiqi Huoxue recipe improves the injured heart function maybe through inhibition of ER stress response pathway, which is a promising target in therapy for heart failure.


2017 ◽  
Vol 233 (4) ◽  
pp. 2863-2870 ◽  
Author(s):  
Ahmed Badreddin ◽  
Youssef Fady ◽  
Hamdy Attia ◽  
Mohamed Hafez ◽  
Ahmed Khairallah ◽  
...  

2015 ◽  
Vol 8 (5) ◽  
pp. 643-652 ◽  
Author(s):  
Byambajav Buyandelger ◽  
Catherine Mansfield ◽  
Sawa Kostin ◽  
Onjee Choi ◽  
Angharad M. Roberts ◽  
...  

2004 ◽  
Vol 107 (5) ◽  
pp. 513-517 ◽  
Author(s):  
Roger CORDER ◽  
Richard C. WARBURTON ◽  
Noorafza Q. KHAN ◽  
Ruth E. BROWN ◽  
Elizabeth G. WOOD ◽  
...  

Reduced endothelium-dependent vasodilator responses with increased synthesis of ET-1 (endothelin-1) are characteristics of endothelial dysfunction in heart failure and are predictive of mortality. Identification of treatments that correct these abnormalities may have particular benefit for patients who become refractory to current regimens. Hawthorn preparations have a long history in the treatment of heart failure. Therefore we tested their inhibitory effects on ET-1 synthesis by cultured endothelial cells. These actions were compared with that of GSE (grape seed extract), as the vasoactive components of both these herbal remedies are mainly oligomeric flavan-3-ols called procyanidins. This showed extracts of hawthorn and grape seed were equipotent as inhibitors of ET-1 synthesis. GSE also produced a potent endothelium-dependent vasodilator response on preparations of isolated aorta. Suppression of ET-1 synthesis at the same time as induction of endothelium-dependent vasodilation is a similar response to that triggered by laminar shear stress. Based on these results and previous findings, we hypothesize that through their pharmacological properties procyanidins stimulate a pseudo laminar shear stress response in endothelial cells, which helps restore endothelial function and underlies the benefit from treatment with hawthorn extract in heart failure.


Biofeedback ◽  
2013 ◽  
Vol 41 (1) ◽  
pp. 39-42
Author(s):  
Jan B. Newman

Emotions have been connected to the heart throughout the ages, yet they have been largely discounted as playing an important role in heart disease. There is mounting evidence that anxiety, anger, depression, and stress play significant contributing roles in cardiac diseases. These emotional states, coronary artery disease, and heart failure have physiology consistent with the ongoing stress response characterized by parasympathetic withdrawal and sympathetic activation. Pharmacological therapies, vagal stimulation, and sympathetic ablation have shown efficacy in these diseases. Similar results can be obtained by biofeedback therapies.


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