Epigallocatechin, a green tea polyphenol, attenuates myocardial ischemia reperfusion injury in rats

被引:140
作者
Aneja, R
Hake, PW
Burroughs, TJ
Denenberg, AG
Wong, HR
Zingarelli, B
机构
[1] Childrens Hosp, Med Ctr, Div Crit Care Med, Dept Pediat, Cincinnati, OH 45229 USA
[2] Univ Cincinnati, Coll Med, Cincinnati, OH 45229 USA
关键词
D O I
10.2119/2004-00032.Aneja
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epigallocatechin-3-gallate (EGCG) is the most prominent catechin in green tea. EGCG has been shown to modulate numerous molecular targets in the setting of inflammation and cancer. These molecular targets have also been demonstrated to be important participants in reperfusion injury, hence this study examines the effects of EGCG in myocardial reperfusion injury. Male Wistar rats were subjected to myocardial ischemia (30 min) and reperfusion (up to 2 h). Rats were treated with EGCG (10 mg/kg intravenously) or with vehicle at the end of the ischemia period followed by a continuous infusion (EGCG 10 mg/kg/h) during the reperfusion period. In vehicle-treated rats, extensive myocardial injury was associated with tissue neutrophil infiltration as evaluated by myeloperoxidase activity, and elevated levels of plasma creatine phosphokinase. Vehicle-treated rats also demonstrated increased plasma levels of interleukin-6. These events were associated with cytosol degradation of inhibitor kappaB-alpha activation of IkappaB kinase, phosphorylation of c-Jun, and subsequent activation of nuclear factor-kappaB and activator protein-1 in the infarcted heart. In vivo treatment with EGCG reduced myocardial damage and myeloperoxidase activity. Plasma IL-6 and creatine phosphokinase levels were decreased after EGCG administration. This beneficial effect of EGCG was associated with reduction of nuclear factor-kappaB and activator protein-1 DNA binding. The results of this study suggest that EGCG is beneficial for the treatment of reperfusion-induced myocardial damage by inhibition of the NF-kappaB and AP-1 pathway.
引用
收藏
页码:55 / 62
页数:8
相关论文
共 54 条
[1]   Green tea constituent epigallocatechin-3-gallate and induction of apoptosis and cell cycle arrest in human carcinoma cells [J].
Ahmad, N ;
Feyes, DK ;
Nieminen, AL ;
Agarwal, R ;
Mukhtar, H .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1997, 89 (24) :1881-1886
[2]   Reperfusion injury: Experimental evidence and clinical implications [J].
Ambrosio, G ;
Tritto, I .
AMERICAN HEART JOURNAL, 1999, 138 (02) :S69-S75
[3]  
Beauparlant Pierre, 1996, Cytokine and Growth Factor Reviews, V7, P175, DOI 10.1016/1359-6101(96)00020-2
[4]   Inhibition of inducible nitric oxide synthase gene expression and enzyme activity by epigallocatechin gallate, a natural product from green tea [J].
Chan, MMY ;
Fong, D ;
Ho, CT ;
Huang, HI .
BIOCHEMICAL PHARMACOLOGY, 1997, 54 (12) :1281-1286
[5]   A green tea-derived polyphenol, epigallocatechin-3-gallate, inhibits IκB kinase activation and IL-8 gene expression in respiratory epithelium [J].
Chen, PC ;
Wheeler, DS ;
Malhotra, V ;
Odoms, K ;
Denenberg, AG ;
Wong, HR .
INFLAMMATION, 2002, 26 (05) :233-241
[6]   Tea is good for the heart [J].
Cheng, TO .
ARCHIVES OF INTERNAL MEDICINE, 2000, 160 (15) :2397-2397
[7]  
CHOW HH, 2003, CLIN CANCER RES, V9, P32
[8]   Global ischemia activates nuclear factor-kappa B in forebrain neurons of rats [J].
Clemens, JA ;
Stephenson, DT ;
Smalstig, EB ;
Dixon, EP ;
Little, SP .
STROKE, 1997, 28 (05) :1073-1080
[9]   A cytokine-responsive I kappa B kinase that activates the transcription factor NF-kappa B [J].
DiDonato, JA ;
Hayakawa, M ;
Rothwarf, DM ;
Zandi, E ;
Karin, M .
NATURE, 1997, 388 (6642) :548-554
[10]   Neutrophil, restraint by green tea:: Inhibition of inflammation, associated angiogenesis, and pulmonary fibrosis [J].
Donà, M ;
Dell'Aica, I ;
Calabrese, F ;
Benelli, R ;
Morini, M ;
Albini, A ;
Garbisa, S .
JOURNAL OF IMMUNOLOGY, 2003, 170 (08) :4335-4341