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 ◽  
...  

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

2011 ◽  
Vol 18 (2) ◽  
pp. 123-130 ◽  
Author(s):  
Leticia Martín-Cordero ◽  
Juan José García ◽  
María Dolores Hinchado ◽  
Elena Bote ◽  
Rafael Manso ◽  
...  

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 990
Author(s):  
Mifetika Lukitasari ◽  
Mohammad Saifur Rohman ◽  
Dwi Adi Nugroho ◽  
Mukhamad Nur Kholis ◽  
Nila Aisyah Wahyuni ◽  
...  

Background: Insulin resistance has been independently associated with cardiac diseases. A free fatty acid is recently known to induce cardiac insulin resistance due to low-grade inflammation. Therefore, the improvement of free fatty acid levels can also improve cardiac insulin resistance. This study investigated the combination of green tea and decaffeinated-light roasted green coffee extract in improvement of free fatty acid-induced cardiac insulin resistance by improving the adiponectin/FAS pathway. Methods: This study used 25 males Sprague-Dawley rats induced by a high-fat high sucrose diet and injection of low dose streptozotocin to make a metabolic syndrome (MS) rat model and standard chow as healthy control rats. The MS rats were treated with green tea (200 mg/ b. w.), decaffeinated-light roasted green coffee (300 mg/ b. w.), and the combination of both extracts in 9 weeks. Experimental groups in this study were divided into 5 groups: 1) MS (HFHS diet + STZ) group, 2) NC (normal chow) group, 3) GT (green tea extract) group, 4) GC (decaffeinated-light roasted green coffee extract), 5) CM (combination of both extracts) group. Adiponectin and HOMA-IR level was analysed using ELISA, and the gene expression of Adipo-R1, FAS, PI3K, PDK1, Akt, GLUT4 was measured by RT-PCR. Results: The combination of green tea and decaffeinated-light roasted green coffee showed synergistic effects in improving FFA levels. The adiponectin/FAS pathway was attenuated in the CM group. Moreover, the combination also showed improvement in cardiac insulin resistance markers such as IRS1/2, PI3K, PDK1, Akt, and GLUT4. Conclusions:  The combination of green tea and decaffeinated-light roasted green coffee extract improved cardiac insulin resistance better than green tea and green coffee extract administration alone by reducing free fatty acids levels through adiponectin/FAS pathway modulation.


2021 ◽  
Vol 22 (3) ◽  
pp. 1022
Author(s):  
Tatyana P. Makalish ◽  
Ilya O. Golovkin ◽  
Volodymyr V. Oberemok ◽  
Kateryna V. Laikova ◽  
Zenure Z. Temirova ◽  
...  

The urgency of the search for inexpensive and effective drugs with localized action for the treatment of rheumatoid arthritis continues unabated. In this study, for the first time we investigated the Cytos-11 antisense oligonucleotide suppression of TNF-α gene expression in a rat model of rheumatoid arthritis induced by complete Freund’s adjuvant. Cytos-11 has been shown to effectively reduce peripheral blood concentrations of TNF-α, reduce joint inflammation, and reduce pannus development. The results achieved following treatment with the antisense oligonucleotide Cytos-11 were similar to those of adalimumab (Humira®); they also compared favorably with those results, which provides evidence of the promise of drugs based on antisense technologies in the treatment of this disease.


2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Albert Gao ◽  
Lauren D Black

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.


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