Abstract

This study was designed to investigate whether bamboo culm extract (BCE) supplementation may ameliorate risk factors of cardiovascular diseases, such as hypercholesterolemia. Oxidative stress and inflammatory mediators in plasma, livers of C57BL/6 mice fed high-cholesterol diet and calf pulmonary artery endothelial (CPAE) cells. Briefly, C57BL/6 mice were fed the high-cholesterol diet which was supplemented with 1% (w/w), or 3% (w/w) of BCE for 16 weeks. The concentration of total cholesterol, LDL-cholesterol, HDL-cholesterol level and atherogenic index were measured. Plasma TEAC value, hepatic thiobarbituric acid reactive substances (TBARS), protein carbonyl values and hepatic antioxidant enzyme activities, such as Cu,Zn-superoxide dismutase (SOD), Mn-SOD, glutathione peroxidase (GSH-Px), GSH reductase and catalase were determined. In addition, hepatic nuclear factor kappa B activities were detected. In the calf pulmonary artery endothelial (CPAE) cells stimulated with lipopolysaccharide, the expression of vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1) were measured. Plasma cholesterol level was decreased, while HDL-cholesterol was increased, thus atherogenic index was lowered in BCE-supplemented animals. Plasma trolox equivalent and hepatic thiobarbituric acid reactive substances and protein carbonyl values were lowered significantly in BCE groups (p<0.05) in a dose-dependent manner. Hepatic antioxidative enzyme activities, such as Cu,Zn-superoxide dismutase (SOD), Mn-SOD, glutathione peroxidase (GSH-P), GSH reductase, and catalase were elevated in mice fed BCE-supplemented diets (p<0.05). Nuclear factor kappa B activities of livers and vascular cell adhesion molecule-1 and intracellular cell adhesion molecule-1 expressions in CPAE cells stimulated with lipopolysaccharide were significantly lowered in BCE groups (p<0.05). These results suggest that BCE supplementation may modulate lipoprotein composition and attenuate oxidative stress by elevated antioxidative processes, thus suppressing inflammatory mediator activation as possible mechanism of its anti-atherogenic effect.

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