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Taurine reduces high glucose induced leukocyte–endothelial interactions via down‐regulation of ICAM‐1
Author(s) -
Casey R. G.,
Chen G.,
Joyce M.,
Kelly C. J.,
BouchierHayes D. J.
Publication year - 2002
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1046/j.1469-7580.2002.00047_9.x
Subject(s) - taurine , endothelial dysfunction , endothelium , nitric oxide , medicine , endothelial stem cell , endocrinology , biochemistry , chemistry , biology , pharmacology , amino acid , in vitro
Taurine is a semiessential amino acid and naturally occurring antioxidant. One of its main roles is to protect tissues against attack by chlorinated oxidants particularly hypochlorous acid (HOCl). It is found in high concentrations in neutrophils and previous studies showed it possesses potent antimicrobial properties and attenuates high glucose induced endothelial cell apoptosis. In humans taurine has been shown to up‐regulate constitutive nitric oxide synthase (cNOS), a known cytoprotector. No reported studies to date have looked at the possible therapeutic role of taurine in preventing diabetic endothelial dysfunction. We therefore hypothesised that taurine would attenuate the microvascular changes associated with hyperglycaemia in an animal model through alteration of leucocyte–endothelial interactions. Male Sprague Dawley rats were randomised into control, hyperglycaemia, and taurine + hyperglycaemia groups. Taurine was gavaged (200 mg/kg) for 5 d prior to the experiment. Hyperglycaemia was established by intravenous infusion of 50% glucose. Blood glucose reached a steady state of 3 times baseline at 30 min. Using intravital microscopy leukocyte rolling, adhesion and transendothelial migration was determined in mesenteric postcapillary venules for 3 h. Intracellular adhesion molecule‐1 (ICAM‐1) was immunohistochemically graded using a scoring system to determine the expression in mesenteric tissue. Taurine pretreatment significantly attenuates leukocyte‐endothelial adhesion and transendothelial migration following acute hyperglycaemia but not leukocyte rolling velocity. The mechanism by which taurine protects against these effects is in part by inhibition of ICAM‐1 expression .Results at 120 min ( n = 5/group) Control Hyperglycaemia Taurine + HyperglycaemiaLeukocyte rolling velocity (m/s) 49.5 (4.5) 30.4 (6.4) 45.4 (5.5) Leukocyteadhesion (/100(m)) 2.25 (1.70) * 44.0 (10.5) 9.25 (2.3) * Transendothelialmigration (/field) 6.5 (1.3) * 76.8 (20.7) 12.25 (5.9) * Expression ofICAM‐1 (at 180 mins) 1.05 (0.40) * 2.9 (0.4) 1.1 (0.3) *Data are expressed as mean (SEM). Analysis with anova and post Scheffe hoc test. * P < 0.05 vs. Hyperglycaemia.