Cardiac Fibrosis Attenuation by Chlorogenic Acid and Epigallocatechin-Gallate Mediated by Suppression of Galectin-3 Gene Expression and Collagen Deposition in Rat Metabolic Syndrome Model

2021 ◽  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Chlorogenic Acid ◽  
Cardiac Fibrosis ◽  
Epigallocatechin Gallate ◽  
Collagen Deposition ◽  
Galectin 3 ◽  
Metabolic Syndrome Model

scholarly journals Improvement of Cardiac Fibrosis Biomarkers through Inflammation Inhibition by Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Administration in Metabolic Syndrome Rat Model

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1013
Author(s):  
Mifetika Lukitasari ◽  
Mohammad Saifur Rohman ◽  
Dwi Adi Nugroho ◽  
Nila Aisyah Wahyuni ◽  
Mukhamad Nur Kholis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Green Tea ◽  
Rat Model ◽  
Cardiac Fibrosis ◽  
Significant Risk ◽  
Green Coffee ◽  
The Metabolic Syndrome ◽  
Tnf Α ◽  
Tgf Β1

Background: Metabolic syndrome is a significant risk factor for cardiovascular diseases. Green tea and green coffee extracts, antioxidant and anti-inflammatory agents may participate in metabolic syndrome-induced cardiac fibrosis alleviation. However, the effect of combination of those extracts still needs exploration. Therefore, this study investigated the effect of green tea and decaffeinated light roasted green coffee extracts and their combination in metabolic syndrome-induced cardiac fibrosis rats. Methods: Metabolic syndrome rat model was i1nduced through high-fat high sucrose diets feeding for 8 weeks and injection of low dose streptozotocin at the 2nd week. The metabolic syndrome rats were divided into 4 experimental groups metabolic syndrome rats (MS); metabolic syndrome rats treated with 300 mg/ kg b.w green tea extract (GT); metabolic syndrome rats treated with 200 mg/ kg b.w decaffeinated light roasted green coffee extract (GC); metabolic syndrome rats treated with the combination of the two extracts (CE); and a normal control (NC) group was added. Angiotensin 2 level was analyzed by ELISA method. Gene expression of NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma were analyzed by touchdown polymerase chain reaction methods. Results: Metabolic syndrome rats treated with green tea and decaffeinated light roasted green coffee significantly decreased angiotensin-2 serum level and cardiac inflammation and fibrosis gene expression level (NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma). More significant alleviation was observed in the combination group. Conclusion: This study suggested that combination of green tea and decaffeinated light roasted green coffee extracts showed better improvement in metabolic syndrome-induced cardiac fibrosis rat model compared to that of single extract administration through inflammation inhibition

scholarly journals Biomarkers in patients with myocardial fibrosis

2017 ◽  
Vol 12 (1) ◽  
pp. 337-344 ◽  
Author(s):  
Zhe An ◽  
Guang Yang ◽  
Haikuo Zheng ◽  
Wei Nie ◽  
Guohui Liu
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Early Detection ◽  
Myocardial Fibrosis ◽  
Gold Standard ◽  
Cardiac Fibrosis ◽  
Collagen Deposition ◽  
Circulating Biomarkers ◽  
Galectin 3 ◽  
Noninvasive Assessment

AbstractMyocardial fibrosis is observed in many cardiovascular diseases including hypertension, heart failure and cardiomyopathy. Myocardial fibrosis has been proved to be reversible and treatable only under timely intervention, which makes early detection and assessment of fibrosis crucial. Aside from tissue biopsy as the gold standard for the diagnosis of myocardial fibrosis, circulating biomarkers have been adopted as noninvasive assessment of this lesion. Dysregulated collagen deposition is thought to be the major cause of myocardial fibrosis. Collagens, procollagens, TGF-β, TIMP, galectin-3, and microRNAs are thought to be indicators of myocardial fibrosis. In this review, we summarize the molecules that are frequently used as biomarkers in diagnosis of cardiac fibrosis. Mechanisms of fibrosis that they take part in are also introduced.

Galectin-3 in Heart Failure – Linking Fibrosis, Remodelling and Progression

2010 ◽  
Vol 6 (2) ◽  
pp. 33 ◽  
Author(s):  
Christopher R deFilippi ◽  
G Michael Felker ◽  
◽  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Risk Stratification ◽  
Cardiac Fibrosis ◽  
The Elderly ◽  
Preserved Ejection Fraction ◽  
Heart Failure Patients ◽  
Large Populations ◽  
Galectin 3

For many with heart failure, including the elderly and those with a preserved ejection fraction, both risk stratification and treatment are challenging. For these large populations and others there is increasing recognition of the role of cardiac fibrosis in the pathophysiology of heart failure. Galectin-3 is a novel biomarker of fibrosis and cardiac remodelling that represents an intriguing link between inflammation and fibrosis. In this article we review the biology of galectin-3, recent clinical research and its application in the management of heart failure patients.

Metforminium Decavanadate (MetfDeca) Treatment Ameliorates Hippocampal Neurodegeneration and Recognition Memory in a Metabolic Syndrome Model

2021 ◽  
Vol 46 (5) ◽  
pp. 1151-1165
Author(s):  
Alfonso Diaz ◽  
Guadalupe Muñoz-Arenas ◽  
Berenice Venegas ◽  
Rubén Vázquez-Roque ◽  
Gonzalo Flores ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Recognition Memory ◽  
Metabolic Syndrome Model ◽  
Hippocampal Neurodegeneration

Study of DYRK1B gene expression and its association with metabolic syndrome in a small cohort of Egyptians

2021 ◽  
Author(s):  
Yara Ahmed Mohamed ◽  
H. M. Hassaneen ◽  
Mohamed A. El-Dessouky ◽  
Gehan Safwat ◽  
Naglaa Abu-Mandil Hassan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Small Cohort

scholarly journals Pathophysiological, Genetic and Gene Expression Features of a Novel Rodent Model of the Cardio-Metabolic Syndrome

PLoS ONE ◽  
2008 ◽  
Vol 3 (8) ◽  
pp. e2962 ◽  
Author(s):  
Robert H. Wallis ◽  
Stephan C. Collins ◽  
Pamela J. Kaisaki ◽  
Karène Argoud ◽  
Steven P. Wilder ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Rodent Model

Abstract 367: Lysyl Oxidase Expression by Cardiac Fibroblasts is Regulated by Integrin-mediated Signaling

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Albert Gao ◽  
Lauren D Black
Keyword(s):  
Gene Expression ◽  
Cardiac Fibrosis ◽  
Lysyl Oxidase ◽  
Cardiac Fibroblasts ◽  
Therapeutic Strategies ◽  
Expression Of Genes ◽  
Adverse Remodeling ◽  
Novel Therapeutic Strategies ◽  
Free Media ◽  
Tgf Β1

Cardiac fibrosis following myocardial infarction (MI) leads to reduced cardiac function, and contributes to heart failure and mortality. Recent studies shown the extent of adverse remodeling may be mitigated by therapeutic strategies which regulate cardiac fibroblast mediated-remodeling. Since cross-linking by lysyl oxidase (LOX) increases following MI and alters the mechanical properties of the infarct, it is critical to characterize how its expression is regulated by CFs post-MI. While LOX expression is attributable to TGF-β1 signaling, we hypothesize that changes in the stiffness and composition of the ECM can also alter LOX expression via integrin-mediated signaling. To investigate this, we isolated CFs from healthy left ventricle (LV) and infarcted cardiac fibroblasts (ICFs) from 1 week post-MI LV and cultured them on tissue culture plastic (TCP) and collagen I-coated plates (COL) in serum-free media for 48 hours to assess the expression of genes associated with LOX signaling, fibrosis, and myofibroblast activation. Our results show an upregulation of LOX gene expression in both CFs and ICFs when cultured on COL and this is further emphasized with the presence of TGF-β1 (Fig. 1A). Gene expression of col1α1, integrin β1 subunit and αSMA (Fig. 1B-D) also exhibit similar upregulation. Ongoing studies will investigate how altered substrate stiffness and composition affect gene expression of LOX and other genes associated with fibrosis. By understanding the effect of the physical microenvironment on the expression of fibrotic genes including LOX, we aim to develop novel therapeutic strategies to attenuate cardiac fibrosis and thus improve cardiac recovery following MI.

Sign in / Sign up

Export Citation Format

Share Document