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Tea polyphenols regulate key mediators on inflammatory cardiovascular diseases.

Suzuki J, Isobe M, Morishita R, Nagai R - Mediators Inflamm. (2009)

Bottom Line: Tea polyphenols known as catechins are key components with many biological functions, including anti-inflammatory, antioxidative, and anticarcinogenic effects.These effects are induced by the suppression of several inflammatory factors including nuclear factor-kappa B (NF-kappaB).From our results, catechins are potent agents for the treatment and prevention of inflammation-related cardiovascular diseases because they are critically involved in the suppression of proinflammatory signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan. junichisuzuki-circ@umin.ac.jp

ABSTRACT
Tea polyphenols known as catechins are key components with many biological functions, including anti-inflammatory, antioxidative, and anticarcinogenic effects. These effects are induced by the suppression of several inflammatory factors including nuclear factor-kappa B (NF-kappaB). While these characteristics of catechins have been well documented, actions of catechins as mediators on inflammation-related cardiovascular diseases have not yet been well investigated. In this article, we reviewed recent papers to reveal the anti-inflammatory effects of catechins in cardiovascular diseases. In our laboratory, we performed oral administration of catechins into murine and rat models of cardiac transplantation, myocarditis, myocardial ischemia, and atherosclerosis to reveal the effects of catechins on the inflammation-induced ventricular and arterial remodeling. From our results, catechins are potent agents for the treatment and prevention of inflammation-related cardiovascular diseases because they are critically involved in the suppression of proinflammatory signaling pathways.

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Zymography of myocardial ischemia. Gelatin zymography showed that increased gelatinase (MMP-2 and MMP-9) activity was observed in hearts in the non-treated ischemia group.  However, this enhanced gelatinase activity was decreased by catechin administration (20 mg/kg/day, THEA-FLAN 90S).
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fig2: Zymography of myocardial ischemia. Gelatin zymography showed that increased gelatinase (MMP-2 and MMP-9) activity was observed in hearts in the non-treated ischemia group. However, this enhanced gelatinase activity was decreased by catechin administration (20 mg/kg/day, THEA-FLAN 90S).

Mentions: Myocardial ischemia and ventricular remodeling causes significant damage leading to severe heart failure. It has been known that NF-κB related inflammation is enhanced by ischemia and reperfusion of myocardium; the activated NF-κB induces MMPs. Thus, decoy against NF-κB reduces myocardial inflammation induced by ischemia/reperfusion injury [26]. Since MMPs are key components in the positive feedback loop of heart remodeling, the inhibition is an effective therapy for myocardial reperfusion injury [27–30]. It is also well known that catechins suppress several inflammatory factors including MMPs induced by NF-κB [10]. To clarify the role of catechins on the ischemic hearts, we made a rat myocardial ischemia model by ligation of the left anterior descending coronary artery and this was continued for 28 days. After ischemic injury, the nontreated ischemia group showed significant decline of blood pressure compared to non-treated sham-operated group. However, the catechin (20 mg/kg/day, THEA-FLAN 90S) administration suppressed the decline of the blood pressure compared to that of non-treated ischemia group on days 14 and 21. Pathologically, the anterior wall of the hearts was completely fibrotic and remaining area showed interstitial fibrosis and cell infiltration. However, catechin-treated hearts showed significantly less infarct size, infarct length, left ventricular circumference, and left ventricular inner diameter than those in the non-treated ischemia group. Immunohistochemically, increased numbers of CD4, CD8, CD11b ICAM-1, and ED-1 positive infiltrating cells were observed in the non-treated ischemia group, while the catechin administration suppressed the numbers significantly. Finally, to reveal the role of MMPs, the infarct region and myocardium were separated under a dissecting microscope and they were used zymography as previously reported. This showed that increased gelatinase (MMP-2 and MMP-9) activity was observed in hearts in the non-treated ischemia group. However, this enhanced gelatinase activity was decreased by catechin administration (Figure 2). In summary of myocardial ischemia, we revealed that catechins prevented ventricular remodeling after ischemic injury due to the suppression of proinflammatory factors including MMPs.


Tea polyphenols regulate key mediators on inflammatory cardiovascular diseases.

Suzuki J, Isobe M, Morishita R, Nagai R - Mediators Inflamm. (2009)

Zymography of myocardial ischemia. Gelatin zymography showed that increased gelatinase (MMP-2 and MMP-9) activity was observed in hearts in the non-treated ischemia group.  However, this enhanced gelatinase activity was decreased by catechin administration (20 mg/kg/day, THEA-FLAN 90S).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2712737&req=5

fig2: Zymography of myocardial ischemia. Gelatin zymography showed that increased gelatinase (MMP-2 and MMP-9) activity was observed in hearts in the non-treated ischemia group. However, this enhanced gelatinase activity was decreased by catechin administration (20 mg/kg/day, THEA-FLAN 90S).
Mentions: Myocardial ischemia and ventricular remodeling causes significant damage leading to severe heart failure. It has been known that NF-κB related inflammation is enhanced by ischemia and reperfusion of myocardium; the activated NF-κB induces MMPs. Thus, decoy against NF-κB reduces myocardial inflammation induced by ischemia/reperfusion injury [26]. Since MMPs are key components in the positive feedback loop of heart remodeling, the inhibition is an effective therapy for myocardial reperfusion injury [27–30]. It is also well known that catechins suppress several inflammatory factors including MMPs induced by NF-κB [10]. To clarify the role of catechins on the ischemic hearts, we made a rat myocardial ischemia model by ligation of the left anterior descending coronary artery and this was continued for 28 days. After ischemic injury, the nontreated ischemia group showed significant decline of blood pressure compared to non-treated sham-operated group. However, the catechin (20 mg/kg/day, THEA-FLAN 90S) administration suppressed the decline of the blood pressure compared to that of non-treated ischemia group on days 14 and 21. Pathologically, the anterior wall of the hearts was completely fibrotic and remaining area showed interstitial fibrosis and cell infiltration. However, catechin-treated hearts showed significantly less infarct size, infarct length, left ventricular circumference, and left ventricular inner diameter than those in the non-treated ischemia group. Immunohistochemically, increased numbers of CD4, CD8, CD11b ICAM-1, and ED-1 positive infiltrating cells were observed in the non-treated ischemia group, while the catechin administration suppressed the numbers significantly. Finally, to reveal the role of MMPs, the infarct region and myocardium were separated under a dissecting microscope and they were used zymography as previously reported. This showed that increased gelatinase (MMP-2 and MMP-9) activity was observed in hearts in the non-treated ischemia group. However, this enhanced gelatinase activity was decreased by catechin administration (Figure 2). In summary of myocardial ischemia, we revealed that catechins prevented ventricular remodeling after ischemic injury due to the suppression of proinflammatory factors including MMPs.

Bottom Line: Tea polyphenols known as catechins are key components with many biological functions, including anti-inflammatory, antioxidative, and anticarcinogenic effects.These effects are induced by the suppression of several inflammatory factors including nuclear factor-kappa B (NF-kappaB).From our results, catechins are potent agents for the treatment and prevention of inflammation-related cardiovascular diseases because they are critically involved in the suppression of proinflammatory signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan. junichisuzuki-circ@umin.ac.jp

ABSTRACT
Tea polyphenols known as catechins are key components with many biological functions, including anti-inflammatory, antioxidative, and anticarcinogenic effects. These effects are induced by the suppression of several inflammatory factors including nuclear factor-kappa B (NF-kappaB). While these characteristics of catechins have been well documented, actions of catechins as mediators on inflammation-related cardiovascular diseases have not yet been well investigated. In this article, we reviewed recent papers to reveal the anti-inflammatory effects of catechins in cardiovascular diseases. In our laboratory, we performed oral administration of catechins into murine and rat models of cardiac transplantation, myocarditis, myocardial ischemia, and atherosclerosis to reveal the effects of catechins on the inflammation-induced ventricular and arterial remodeling. From our results, catechins are potent agents for the treatment and prevention of inflammation-related cardiovascular diseases because they are critically involved in the suppression of proinflammatory signaling pathways.

Show MeSH
Related in: MedlinePlus