Comparison of protective effects of aspirin, D-penicillamine and vitamin E against high glucose-mediated toxicity in cultured endothelial cells

被引:14
作者
Zhang, Jing [1 ]
Slevin, Mark [1 ]
Duraisamy, Yasotha [1 ]
Gaffney, John [1 ]
Smith, Christopher A. [1 ]
Ahmed, Nessar [1 ]
机构
[1] Manchester Metropolitan Univ, Sch Biol Chem & Hlth Sci, Manchester M1 5GD, Lancs, England
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2006年 / 1762卷 / 05期
关键词
glycation; advanced glycation endproduct; aspirin; D-penicillamine; vitamin E; wound healing; endothelial cell; diabetes; antioxidant;
D O I
10.1016/j.bbadis.2006.02.004
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
This study compared the protective effects of three different anti-glycation compounds, aspirin, D-penicillamine and vitamin E, against high glucose and advanced glycation endproduct (AGE) mediated toxicity in cultured bovine aortic endothelial cells using two approaches. Their proliferation was assessed in culture in different concentrations of glucose (5.5-100 mmol/1) with and without these inhibitors. A monolayer of cultured endothelial cells was wounded and recovery at the wound site was measured following exposure to different concentrations of glucose with and without inhibitors. The ability of these compounds to protect cultured endothelial cells following exposure to bovine serum albumin-derived advanced glycation endproducts (BSA-AGE) was also studied. Addition of glucose to cultured endothelial cells inhibited their proliferation in a dose dependent manner. All three compounds protected against the anti-proliferative effects of high glucose, with vitamin E being the most effective. The migration of cultured endothelial cells following wounding was inhibited by increasing concentrations of glucose but was maintained in the presence of all three anti-glycation compounds with vitamin E, again giving the greatest protection. Vitamin E was also the most effective at protecting against the anti-proliferative effects of BSA-AGE. D-penicillamine was not as effective as vitamin E whereas aspirin offered no significant protection against AGE-induced cellular toxicity. Our studies suggest that compounds, such as vitamin E, with combined antiglycation and antioxidant properties offer maximum therapeutic potential in protection against high glucose and AGE-mediated cellular toxicity. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:551 / 557
页数:7
相关论文
共 47 条
  • [1] Advanced glycation endproducts - role in pathology of diabetic complications
    Ahmed, N
    [J]. DIABETES RESEARCH AND CLINICAL PRACTICE, 2005, 67 (01) : 3 - 21
  • [2] Advanced glycosylation end products in diabetic renal and vascular disease
    Bucala, R
    Vlassara, H
    [J]. AMERICAN JOURNAL OF KIDNEY DISEASES, 1995, 26 (06) : 875 - 888
  • [3] Tobacco smoke is a source of toxic reactive glycation products
    Cerami, C
    Founds, H
    Nicholl, I
    Mitsuhashi, T
    Giordano, D
    Vanpatten, S
    Lee, A
    AlAbed, Y
    Vlassara, H
    Bucala, R
    Cerami, A
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (25) : 13915 - 13920
  • [4] CERIELLO A, 1988, DIABETES METAB, V14, P40
  • [5] GLYCATION OF HUMAN LENS CRYSTALLINS - EFFECT OF AGE AND ASPIRIN TREATMENT
    CHERIAN, M
    ABRAHAM, EC
    [J]. OPHTHALMIC RESEARCH, 1993, 25 (06) : 349 - 354
  • [6] Toxic action of advanced glycation end products on cultured retinal capillary pericytes and endothelial cells: Relevance to diabetic retinopathy
    Chibber, R
    Molinatti, PA
    Rosatto, N
    Lambourne, B
    Kohner, EM
    [J]. DIABETOLOGIA, 1997, 40 (02) : 156 - 164
  • [7] CRABBE MJC, 1998, MAILLARD REACTION FO, P268
  • [8] CURCIO F, 1992, IN VITRO CELL DEV-AN, V28A, P787
  • [9] DOLGOV VV, 1982, DIABETOLOGIA, V22, P338
  • [10] Aminosalicylic acid reduces the antiproliferative effect of hyperglycaemia, advanced glycation endproducts and glycated basic fibroblast growth factor in cultured bovine aortic endothelial cells: Comparison with aminoguanidine
    Duraisamy, Y
    Gaffney, J
    Slevin, M
    Smith, CA
    Williamson, K
    Ahmed, N
    [J]. MOLECULAR AND CELLULAR BIOCHEMISTRY, 2003, 246 (1-2) : 143 - 153