1041-98 Epigallocatechin-3-gallate inhibits stat-1 activation and protects cardiac myocytes from ischemia/reperfusion-induced apoptosis

[1]  A. Stephanou Activated STAT-1 pathway in the myocardium as a novel therapeutic target in ischaemia/reperfusion injury. , 2003, European cytokine network.

[2]  B. Frei,et al.  Tea Catechins and Polyphenols: Health Effects, Metabolism, and Antioxidant Functions , 2003, Critical reviews in food science and nutrition.

[3]  T. Nagata,et al.  (−)-Epigallocatechin gallate protects against NO stress-induced neuronal damage after ischemia by acting as an anti-oxidant , 2002, Brain Research.

[4]  D. Latchman,et al.  The C‐terminal activation domain of the STAT‐1 transcription enhances ischemia/reperfusion‐induced apoptosis in cardiac myocytes , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[5]  M. Moskowitz,et al.  STAT1 is Activated in Neurons after Ischemia and Contributes to Ischemic Brain Injury , 2002, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[6]  D. Frank,et al.  The role of STATs in apoptosis. , 2002, Current molecular medicine.

[7]  R. Knight,et al.  Different Signaling Pathways Induce Apoptosis in Endothelial Cells and Cardiac Myocytes During Ischemia/Reperfusion Injury , 2002, Circulation research.

[8]  D. Geller,et al.  Complex regulation of human inducible nitric oxide synthase gene transcription by Stat 1 and NF-κB , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[9]  R. Knight,et al.  Distinct initiator caspases are required for the induction of apoptosis in cardiac myocytes during ischaemia versus reperfusion injury , 2001, Cell Death and Differentiation.

[10]  Yibin Wang,et al.  The role of differential activation of p38‐mitogen‐activated protein kinase in preconditioned ventricular myocytes , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[11]  P. Boekstegers,et al.  Involvement of CD95/Apo1/Fas in cell death after myocardial ischemia. , 2000, Circulation.

[12]  S. Suh,et al.  Protective effects of the green tea polyphenol (−)-epigallocatechin gallate against hippocampal neuronal damage after transient global ischemia in gerbils , 2000, Neuroscience Letters.

[13]  D. Latchman,et al.  Opposing actions of STAT-1 and STAT-3 on the Bcl-2 and Bcl-x promoters , 2000, Cell Death and Differentiation.

[14]  T. Yue,et al.  Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion. , 1999, Circulation.

[15]  D. Mochly‐Rosen,et al.  An Inhibitor of p38 Mitogen-activated Protein Kinase Protects Neonatal Cardiac Myocytes from Ischemia* , 1999, The Journal of Biological Chemistry.

[16]  Aseem Kumar,et al.  Defective TNF-α-Induced Apoptosis in STAT1-Null Cells Due to Low Constitutive Levels of Caspases , 1997 .

[17]  K. Yamashita,et al.  EFFECTS OF (‐)‐EPIGALLOCATECHIN‐3‐O‐GALLATE (GREEN TEA TANNIN) ON THE LIFE SPAN OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS , 1995, Clinical and experimental pharmacology & physiology. Supplement.

[18]  S. Mariotto,et al.  Anti-interferon gamma action of epigallocatechin-3-gallate mediated by specific inhibition of STAT1 activation. , 2001, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[19]  E. Roth,et al.  The impact of L-arginine-nitric oxide metabolism on ischemia/reperfusion injury. , 1998, Current opinion in clinical nutrition and metabolic care.