Green tea (Cammellia sinensis) attenuates ventricular remodeling after experimental myocardial infarction

INTERNATIONAL JOURNAL OF CARDIOLOGY

卷:225

Article

Lustosa, Beatriz B.¹  Polegato, Bertha¹  Minicucci, Marcos¹  Rafacho, Bruna¹  Santos, Priscila P.¹  Fernandes, Ana Angelica²  Okoshi, Katashi¹  Batista, Diego¹  Modestoa, Pamela¹  Goncalves, Andrea¹  Pereira, Elenize J.¹  Pires, Vanessa¹  Paiva, Sergio¹  Zornoff, Leonardo¹  Azevedo, Paula S.¹ 

[1] UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Sao Paulo, Brazil

[2] UNESP Univ Estadual Paulista, Inst Biosci, Dept Chem & Biochem, Sao Paulo, Brazil

关键词: Myocardial infarction;    Cardiac remodeling;    Antioxidant;    Green tea;   

DOI  :  10.1016/j.ijcard.2016.09.092

来源: Elsevier

【 摘 要 】

Background: Considering the high morbidity and mortality after myocardial infarction (MI), the study of compounds with potential benefits for cardiac remodeling is reasonable. Green tea (GT) (Cammellia sinensis) is the most consumed beverage in the world. The potential action mechanisms of GT include anti-inflammatory, anti-apoptotic, antioxidant, and lipid-lowering properties. Objective: This study analyzed the effects of GT on cardiac remodeling following coronary occlusion in rats. Methods: Male Wistar rats were divided into four groups: control (C), control green tea (GT), myocardial infarction (MI), and myocardial infarction and green tea (MI-GT). GT and MI-GT were fed with standard chow with 0.25% Polyphenon 60 (Sigma-Aldrich Canada, Oakville, ON, Canada). After 3 months of observation, echocardiographic and isolated heart study, oxidative stress, energy metabolism, serum lipids, extracellular matrix, and apoptosis were evaluated. Results: GT reduced cardiac hypertrophy and improved systolic and diastolic dysfunction. Concerning oxidative stress, GT reduced protein carbonyl, increased Nrf-2, and restored antioxidant enzyme activity to the control pattern. Energy metabolism was affected by MI that presented with lower fatty acid oxidation and accumulation of triacylglycerol, increased serum lipids, impairment of the citric acid cycle, and oxidative phosphorylation. GT stimulated the glucose pathway and mitochondrial function after MI by increasing pyruvate dehydrogenase, Complex I, ATP synthase, and glycogen storage. In addition, MI changed the extracellular matrix including MMP-2 and TIMP-1 activity and increased apoptosis by 3-caspase, all of which were attenuated by GT. Conclusion: GT attenuated cardiac remodeling after MI, associated with improvement in systolic and diastolic dysfunction. Oxidative stress, energy metabolism, apoptosis, and extracellular matrix alterations are all potential mechanisms by which GT may take part. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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