Inhibitory effect of Chinese green tea on endothelial cell-induced LDL oxidation

被引:85
作者
Yang, TTC [1 ]
Koo, MWL [1 ]
机构
[1] Univ Hong Kong, Fac Med, Dept Pharmacol, Hong Kong, Peoples R China
关键词
Chinese green tea; Lung Chen Tea; LDL oxidation; cholesterol; relative electrophoretic mobility; TBARS;
D O I
10.1016/S0021-9150(99)00239-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Green tea has been shown to inhibit Cu2+-induced LDL oxidation and suppress lipoxygenase activity. Since LDL oxidation is a characteristic feature of atherogenesis and lipoxygenase is involved in the disease process, the effect of Lung Chen Tea, a non-fermented Chinese green tea, on LDL oxidation induced by human umbilical cord vascular endothelial cell was investigated in the present study. Lung Chen Tea was extracted with methanol and the dried powder was redissolved in water before extraction with chloroform and then ethyl acetate. Lung Chen Tea, chloroform and ethyl acetate fractions dose-dependently reduced LDL oxidation and decreased its relative electrophoretic mobility (P <0.001) when compared to the oxidized LDL. The lipid peroxidation products, thiobarbituric acid reactive substances, and cellular cholesterol were also significantly lowered by 5 and 10 mu g/ml Lung Chen Tea (P < 0.001) in a dose-dependent manner. The remaining aqueous layer, which was devoid of catechins after chloroform and ethyl acetate extractions, did not prevent LDL oxidation. The results of this study demonstrated that Lung Chen Tea and catechin-rich fractions significantly prevented endothelial cell induced LDL oxidation. The consumption of Lung Chen Tea may therefore lower the risk of coronary heart diseases. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:67 / 73
页数:7
相关论文
共 28 条
[1]   SYSTEMIC ACTIVATION OF 15-LIPOXYGENASE IN HEART, LUNG, AND VASCULAR TISSUES BY HYPERCHOLESTEROLEMIA - RELATIONSHIP TO LIPOPROTEIN OXIDATION AND ATHEROGENESIS [J].
BAILEY, JM ;
MAKHEJA, AN ;
LEE, R ;
SIMON, TH .
ATHEROSCLEROSIS, 1995, 113 (02) :247-258
[2]  
BALLANTYNE FC, 1984, ANN CLIN BIOCHEM, V21, P166, DOI 10.1177/000456328402100302
[3]   ANTIATHEROSCLEROTIC EFFECTS OF ANTIOXIDANTS ARE LESION-SPECIFIC WHEN EVALUATED IN HYPERCHOLESTEROLEMIC NEW-ZEALAND WHITE-RABBITS [J].
BOCAN, TMA ;
MUELLER, SB ;
BROWN, EQ ;
UHLENDORF, PD ;
MAZUR, MJ ;
NEWTON, RS .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 1992, 57 (01) :70-83
[4]   Enhancement of antioxidative ability of rat plasma by oral administration of (-)-epicatechin [J].
Da Silva, EL ;
Piskula, M ;
Terao, J .
FREE RADICAL BIOLOGY AND MEDICINE, 1998, 24 (7-8) :1209-1216
[5]  
Daniel W.W., 1991, BIOSTATISTICS FDN AN
[6]   BIOCHEMICAL, STRUCTURAL, AND FUNCTIONAL-PROPERTIES OF OXIDIZED LOW-DENSITY-LIPOPROTEIN [J].
ESTERBAUER, H ;
DIEBERROTHENEDER, M ;
WAEG, G ;
STRIEGL, G ;
JURGENS, G .
CHEMICAL RESEARCH IN TOXICOLOGY, 1990, 3 (02) :77-92
[7]   MALONDIALDEHYDE ALTERATION OF LOW-DENSITY LIPOPROTEINS LEADS TO CHOLESTERYL ESTER ACCUMULATION IN HUMAN MONOCYTE-MACROPHAGES [J].
FOGELMAN, AM ;
SHECHTER, I ;
SEAGER, J ;
HOKOM, M ;
CHILD, JS ;
EDWARDS, PA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1980, 77 (04) :2214-2218
[8]   LIPOXYGENASE CONTRIBUTES TO THE OXIDATION OF LIPIDS IN HUMAN ATHEROSCLEROTIC PLAQUES [J].
FOLCIK, VA ;
NIVARARISTY, RA ;
KRAJEWSKI, LP ;
CATHCART, MK .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (01) :504-510
[9]  
GAMBLE W, 1978, J LIPID RES, V19, P1068
[10]   BINDING-SITE ON MACROPHAGES THAT MEDIATES UPTAKE AND DEGRADATION OF ACETYLATED LOW-DENSITY LIPOPROTEIN, PRODUCING MASSIVE CHOLESTEROL DEPOSITION [J].
GOLDSTEIN, JL ;
HO, YK ;
BASU, SK ;
BROWN, MS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1979, 76 (01) :333-337