Ginsenoside Rb1 inhibits autophagy through regulation of Rho/ROCK and PI3K/mTOR pathways in a pressure-overload heart failure rat model

2018 ◽  
Vol 70 (6) ◽  
pp. 830-838 ◽  
Author(s):  
Tianrui Yang ◽  
Yunbo Miao ◽  
Tong Zhang ◽  
Ninghui Mu ◽  
Libo Ruan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Rat Model ◽  
Pressure Overload ◽  
Ginsenoside Rb1

scholarly journals Anchored cAMP signalling in progression from hypertrophy to heart failure in a rat model of pressure overload

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P5715-P5715
Author(s):  
S. Soni ◽  
E. Corradini ◽  
R. Van Der Nagel ◽  
M. Boulaksil ◽  
A. J. R. Heck ◽  
...  
Keyword(s):  
Heart Failure ◽  
Rat Model ◽  
Pressure Overload ◽  
Camp Signalling

scholarly journals Effects of Lycium barbarum L. Polysaccharides on Inflammation and Oxidative Stress Markers in a Pressure Overload-Induced Heart Failure Rat Model

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 466 ◽  
Author(s):  
Cristina Pop ◽  
Cristian Berce ◽  
Steliana Ghibu ◽  
Iuliu Scurtu ◽  
Olga Sorițău ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Body Weight ◽  
Rat Model ◽  
Pressure Overload ◽  
Oxidative Stress Markers ◽  
Lycium Barbarum ◽  
Stress Markers ◽  
Anti Inflammatory ◽  
And Oxidative Stress

Despite recent advances in disease management and prevention, heart failure (HF) prevalence is still high. Hypertension, inflammation and oxidative stress are being investigated as important causative processes in HF. L. barbarum L. polysaccharides (LBPs) are widely used for their anti-inflammatory and antioxidant properties. Thus, the aim of the present study was to evaluate the effects of LBPs on inflammation and oxidative stress markers in a pressure overload-induced HF rat model, surgically induced by abdominal aorta banding in Wistar rats (AAB) (n = 28). Also, control rats (n = 10) were subjected to a sham operation. After echocardiographic confirmation of HF (week 24), AAB rats were divided into three groups: rats treated with LBPs for 12 weeks: 100 mg/kg body weight /day (AAB_100, n = 9), 200 mg/kg body weight /day (AAB_200, n = 7) and no-treatment group (control AAB, n = 12). After 12 weeks of treatment with LBPs, the decline of cardiac function was prevented compared to the control AAB rats. Treatment with 200 mg/kg body weight /day LBPs significantly reduced the inflammation as seen by cytokine levels (IL-6 and TNF-α) and the plasma lipid peroxidation, as seen by malondialdehyde levels. These results suggest that LBPs present anti-inflammatory and antioxidant effects with utility in a HF animal model and encourage further investigation of the cardioprotective effects of these polysaccharides.

653 Frusemide and mortality in a rat model of chronic heart failure

2007 ◽  
Vol 6 (1) ◽  
pp. 139-139
Author(s):  
J SPRINGER ◽  
S STRASSBURG ◽  
S PALUS ◽  
B BOCKMEYER ◽  
Y AKASHI ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Rat Model

Cardiac insulin resistance as a common feature of pressure overload- and myocardial infarction-induced heart failure

2010 ◽  
Vol 58 (S 01) ◽  
Author(s):  
PA Amorim ◽  
TD Nguyen ◽  
A Schrepper ◽  
A Köppen ◽  
Y Shingu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Insulin Resistance ◽  
Pressure Overload

Pressure overload induced heart failure may be due to impaired respiratory capacity and a defect in complex I

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
M Schwarzer ◽  
M Osterholt ◽  
A Schrepper ◽  
PA Amorim ◽  
T Doenst
Keyword(s):  
Heart Failure ◽  
Complex I ◽  
Pressure Overload ◽  
Respiratory Capacity

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

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