Abstract
Increased reactive oxygen species (ROS) and hyperlipidemia can promote arterial thrombus. We evaluated the potential of a partially hydrolyzed guar gum (PHGG) as dietary fiber on lipid profiles and FeCl3-induced arterial thrombosis in the high fat-diet fed hamsters. Our in vitro results found that PHGG is efficient to scavenge O2-•, H2O2, and HOCl. High fat-diet increased plasma triglyceride, total cholesterol, LDL, VLDL, methylguanidine and dityrosine level and accelerated FeCl3-induced arterial thrombosis formation (from 463 ± 51 to 303 ± 45 sec). Low dose PHGG supplement significantly decreased the total cholesterol, LDL, methylguanidine and dityrosine level and delayed the time for arterial thrombosis formation (528 ± 75 sec). High dose PHGG supplement decreased the level in triglyceride, total cholesterol, LDL and VLDL and further delayed the time for arterial thrombus (671 ± 36 sec). The increased Bax protein and decreased Bcl-2 and HSP-70 protein expression was found in the carotid and femoral arteries of high fat-diet hamsters. Low and high dose of PHGG supplement decreased Bax expression and increased Bcl-2 and HSP-70 protein expression. We found that FeCl3 significantly enhanced intercellular adhesion molecule-1 and 4-hydroxynonenal expression in the endothelial site of damaged artery after 150-sec FeCl3 stimulation. PHGG supplement decreased the endothelial ICAM-1 and 4-hydroxynonenal expression after 150-sec FeCl3 stimulation. Based on these results, we conclude that PHGG supplement can increase antioxidant protein expression and thus decrease oxidative stress induced arterial injury.
Highlights
It is generally accepted that excess reactive oxygen species (ROS) production can cause oxidation of biological macromolecules and produce damage to biological systems [1,2,3,4,5]
4-HNE products and intercellular adhesion molecule-1 (ICAM-1) expression in the carotid artery We considered that the high levels of FeCl3 via Fenton reaction enhanced ROS might promote the expression of ICAM-1 and the accumulation of lipid peroxides, 4hydroxynonenal (4-HNE) in the endothelium for induction of thrombosis within minutes
We found that four weeks of high-fat diet (HF) significantly increased TG, T-CHO, high-density lipoprotein (HDL), LDL and very low-density lipoprotein (VLDL), but not LP(a) level with comparison to the control group
Summary
It is generally accepted that excess reactive oxygen species (ROS) production can cause oxidation of biological macromolecules and produce damage to biological systems [1,2,3,4,5]. Enhanced vascular production of ROS decreases the bioavailability of nitric oxide, impairs vascular relaxation, and promotes leukocytes and platelet adhe-. There is evidence that adhesion of monocytes to the endothelium and transformation of macrophages into foam cells, plaque stability, vasomotor function, platelet aggregation and tendency to thrombosis lead to the development of atherosclerosis and coronary artery disease and can be modified by antioxidants [10,11]. Adhesion of platelet and leukocytes into the vascular endothelial cell by the increased expression of intercellular adhesion molecule-1 (ICAM-1) is a crucial step in thrombosis/atherogenesis [12]. Suppressed expression of ICAM-1 was associated with reduced adherence of monocytes, lymphocytes and platelets to oxidized LDL stimulated endothelial cells [13,12]. Vascular wall protection can be achieved by preventive attachment to the vascular wall of antioxidants and elimination/neutralization of toxic products after their disproportioning [14,15]
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