Decaffeinated Green Tea and Green Coffee Extract Attenuate Cardiac Perivascular Fibrosis in a Metabolic Syndrome Model by Decreasing Fibroblast Growth Factor 23 and Runt-related transcription factor 2 Expression
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Abstract
Metabolic syndrome includes hypertension, obesity, and insulin resistance, which increase the risk of cardiovascular disease (CVD) by up to 50%. This condition activates genes, such as FGF23, GALNT3, and RUNX2, causing heart fibrosis. This study aimed to determine the effect of tea and coffee extract therapy on perivascular fibrosis in the heart of a mouse model of metabolic syndrome and its impact on the expression of fibrosis-related genes such as FGF23, GALNT3, and RUNX2. This study used 25 male Sprague Dawley rats, divided into five groups (n=5): negative control (NORM), positive control (METS), metformin therapy (MFN), green tea and green coffee extract therapy (GTCE), and a combination of both (COMB). The METS samples were fed a high-fat and high-sucrose diet for 18 weeks, followed by a low-dose Streptozotocin injection (30 mf/kgBW) for 11 weeks. The METS model was then administered treatment for 9 weeks. After treatment, the rats were dissected, and the heart organs were analyzed with Masson Trichrome, and FGF23, GALNT3, and RUNX2 mRNA expression was measured by RT-PCR. The results showed that green tea and coffee extracts, alone or in combination with metformin, showed anti-fibrotic effects by reducing collagen deposition (5.87% ± 0.66 and 4.14% ± 0.66) and lowering FGF23 (0.543 ± 0.112 and 0.676 ± 0.159) and RUNX2 (2.716 ± 0.482 and 7.325 ± 0.899). These results suggest that combination extracts exhibit anti-fibrotic effects by reducing collagen deposition in perivascular area. They also suppress pro-fibrotic genes, such as FGF23 and RUNX2, which are involved in cardiac fibrosis.
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