Key result
Chlorogenic acid and epigallocatechin-3-gallate suppress activin-a and collagen-1 expression in metabolic syndrome rats.
Why the study?
Metabolic syndrome contributes to cardiovascular disease and cardiac fibrosis, but the effects of green coffee chlorogenic acid and green tea epigallocatechin-3-gallate on activin-1 and collagen-1 expression were unknown.
Does chlorogenic acid and epigallocatechin-3-gallate reduce activin-a and collagen-1 gene expression in a rat metabolic syndrome model?
Does chlorogenic acid and epigallocatechin-3-gallate reduce activin-a and collagen-1 gene expression in a rat metabolic syndrome model?
p-value: p=0.001 (activin-a), 0.016 (collagen-1)
Chlorogenic acid and epigallocatechin-3-gallate may attenuate cardiac fibrosis in metabolic syndrome by suppressing activin-a and collagen-1 gene expression in a rat model.
Background: Progression in the severity of metabolic syndrome (MetS) contributes to the development of cardiovascular disease. It leads to changes in the histological structure of the heart, known as cardiac fibrosis. Cardiac fibrosis can be identified from the high levels of the profibrotic molecule, such as activin-a and collagen-1. Aim: This study aims to determine the effect of therapy chlorogenic acid (CGA) from green coffee and epigallocatechin-3-gallate (EGCG) from green tea extract on activin-1 and collagen-1 gene expression the rat MetS model. Methods: Twenty-five male MetS rats (Sprague-Dawley) were divided into two control groups and three therapy groups (n=5). The administration of the CGA 200mg/kgbw and EGCG 300mg/kgbw were given orally. After eight weeks of treatment, rats were euthanized, then mRNA expression of activin-1 and collagen-1 were measured. Results: There is a significant effect of giving CGA and EGCG a therapy to suppress the activin-a (P-value= 0.001) and collagen-1 (P-value= 0.016) gene expressions in the rat MetS model. The correlation between the two genes expression shows a positive association. Conclusion: This study shows that CGA and EGCG are potential agents to prevent cardiac fibrosis as a clinical manifestation in metabolic syndrome.
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Chomsy et al. (2022) studied Metabolic syndrome (n=25). Chlorogenic acid (CGA) and epigallocatechin-3-gallate (EGCG) vs. Control groups was evaluated on mRNA expression of activin-a and collagen-1 (p=0.001 (activin-a), 0.016 (collagen-1)). Administration of chlorogenic acid and epigallocatechin-3-gallate significantly suppressed activin-a (P=0.001) and collagen-1 (P=0.016) gene expressions in a rat model of metabolic syndrome.
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