scholarly journals Inflammation‐induced left ventricular fibrosis is partially mediated by tumor necrosis factor‐α

2021 ◽  
Vol 9 (21) ◽  
Author(s):  
Ashmeetha Manilall ◽  
Lebogang Mokotedi ◽  
Sulè Gunter ◽  
Regina Le Roux ◽  
Serena Fourie ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Left Ventricular ◽  
Ventricular Fibrosis ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Pinocembrin Decreases Ventricular Fibrillation Susceptibility in a Rat Model of Depression

2020 ◽  
Vol 11 ◽  
Author(s):  
Tianxin Ye ◽  
Cui Zhang ◽  
Gang Wu ◽  
Weiguo Wan ◽  
Yan Guo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Ventricular Fibrillation ◽  
Tumor Necrosis Factor ◽  
Ventricular Arrhythmias ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ventricular Fibrosis ◽  
Factor Α ◽  
Necrosis Factor

Background: Depression is associated with the increased risk of mortality and morbidity and is an independent risk factor for many cardiovascular diseases. Depression may promote cardiac arrhythmias, but little is known about the mechanisms. Pinocembrin mitigated depressive-like behaviors and exhibited cardioprotective effects in several models; however, whether pinocembrin benefits ventricular arrhythmias in depression models has not been elucidated. Thus, this study was to evaluate the effects of pinocembrin on ventricular fibrillation susceptibility in rat models of depression.Methods: Male Sprague-Dawley rats were randomly assigned into control, control + pinocembrin, MDD (major depressive disorder), and MDP (MDD + pinocembrin) groups, respectively. Depressive-like behaviors, ventricular electrophysiological parameters, electrocardiogram parameters, heart rate variability, ventricular histology, serum norepinephrine, tumor necrosis factor-α, and interleukin-1β were detected. Protein levels in left ventricle were measured by Western blot assays.Results: Compared with the MDD group, pinocembrin significantly mitigated depressive-like behaviors, prolonged ventricular effective refractory period, action potential duration, QT, and corrected QT (QTc) interval, improved heart rate variability, decreased Tpeak–Tend interval, ventricular fibrillation inducibility rate, ventricular fibrosis, ventricular positive nerve densities, and protein expression of tyrosine hydroxylase and growth associated protein-43, reduced serum norepinephrine, tumor necrosis factor-α, interleukin-1β concentrations, and the expression levels of p-IκBα and p-p65, and increased the protein expression of Cx43, Cav1.2, and Kv.4.2 in the MDP group.Conclusion: Pinocembrin attenuates ventricular electrical remodeling, autonomic remodeling, and ion-channel remodeling, lowers ventricular fibrosis, and suppresses depression-induced inflammatory responses, providing new insights in pinocembrin and ventricular arrhythmias in depressed patients.

scholarly journals Pathophysiologically Relevant Concentrations of Tumor Necrosis Factor-α Promote Progressive Left Ventricular Dysfunction and Remodeling in Rats

Circulation ◽  
1998 ◽  
Vol 97 (14) ◽  
pp. 1382-1391 ◽  
Author(s):  
Biykem Bozkurt ◽  
Scott B. Kribbs ◽  
Fred J. Clubb ◽  
Lloyd H. Michael ◽  
Vladimir V. Didenko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Left Ventricular Dysfunction ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals The relationship of cytokine status with left ventricular hypertrophy in patients with arterial hypertension

2019 ◽  
Vol 100 (2) ◽  
pp. 204-213
Author(s):  
T B Zalova ◽  
A G Polupanov ◽  
L G Tsoy ◽  
F T Rysmatova ◽  
I S Sabirov
Keyword(s):  
Tumor Necrosis Factor ◽  
Left Ventricular Hypertrophy ◽  
Tumor Necrosis ◽  
Ventricular Hypertrophy ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Left Ventricular ◽  
Factor Α ◽  
Relationship Of ◽  
Necrosis Factor

Aim. To study the relationship of tumor necrosis factor α and interleukin-10 levels with the presence of left ventricular hypertrophy and myocardial remodeling in patients with arterial hypertension. Metods. 156 patients with hypertension aged 40 to 75 years (mean age 55.8±7.5 years), including 57 women and 99 men were examined. All patients were divided into two groups. Group 1 included 83 patients without left ventricular hypertrophy (55.5±7.5 years), group 2 included 73 patients with left ventricular hypertrophy (56.2±7.8 years), established by echocardiographic signs. All patients in addition to the general clinical examination and biochemical studies had echocardiography and Doppler echocardiography performed, as well as measurement of the concentration of tumor necrosis factor α and interleukin-10 by solid-phase enzyme immunoassay using specialized «Cytokine-Stimulus-Best» kit (Novosibirsk, Russia). Results. The concentration of tumor necrosis factor α in patients without left ventricular hypertrophy was 8.43±1.36 pg/ml and was comparable with the concentration of this cytokine in patients with left ventricular hypertrophy (8.54±1.58 pg/ml, p >0.05). This pattern was typical for both men and women. The concentration of interleukin-10 in both groups was also comparable (15.4±3.6 pg/ml in group 1 and 14.7±3.4 pg/ml in group 2, p >0.05). However, we identified gender-specific features in the relationship of interleukin-10 with the presence of left ventricular hypertrophy in patients with hypertension. Thus, while in women the concentration of cytokine in groups with/without left ventricular hypertrophy did not differ significantly, in men without hypertrophy the level of interleukin-10 of 15.7±3.6 pg/ml, was significantly higher than the value of the same indicator in the group of men with left ventricular hypertrophy (14.8±2.9 pg/ml, p <0.025). Multivariate regression analysis showed that tumor necrosis factor α and interleukin-10 concentrations correlated to left ventricular wall thickness in patients without left ventricular hypertrophy. No such pattern was revealed for patients with hypertrophy. Conclusion. The results demonstrate the modulating role of tumor necrosis factor α and interleukin-10 in myocardial remodeling processes in arterial hypertension.

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