Impact of hyperlipidemia on VCAM-1 expression and cell adhesiveness of endothetium of rats
HE Zhao-chu
Abstract
HE Zhao-chu
Abstract
Objective To study the impact of hyperlipidemia and inflammation on endothelial lesion during the early stage of atheroscterosis.Methods This study included control(basic chow),hyperlipidemic and fenofibrate-treated groups(high-fated diet).Hyperlipidemic model was set up by feeding rats with 4 weeks of atherogenic diet,followed by 16 weeks of treatment in the fenofibrate-treated group [fenofibrate 40 mg/(kg·d)] and without treatment in the hyperlipidemic group.Serum lipid level and NO concentration were measured.Expression of VCAM-1 and cell adhesiveness on aortic endothelium was observed and analyzed by computer-aided system.Results Compared with the control group,hyperlipidemic rats showed lower level of NO and increase in leukocyte accumulation on the endothelial surface,as well as stronger and more extensive endothelial expression of VCAM-1.In contrast,in fenofibrate-treated group,expression of VCAM-1 as well as leukocyte adhesion significantly decreased which was associated with increased NO level.Conclusion NO activity is inhibited by hypertipidemia which facilitates endothelial impairment of VCAM-1.Fenofibrate can prevent atherosclerosis by restoring NO concentration and down-regulating of VCAM-1 expression.
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Objective To study the impact of hyperlipidemia and inflammation on endothelial lesion during the early stage of atheroscterosis.Methods This study included control(basic chow),hyperlipidemic and fenofibrate-treated groups(high-fated diet).Hyperlipidemic model was set up by feeding rats with 4 weeks of atherogenic diet,followed by 16 weeks of treatment in the fenofibrate-treated group [fenofibrate 40 mg/(kg·d)] and without treatment in the hyperlipidemic group.Serum lipid level and NO concentration were measured.Expression of VCAM-1 and cell adhesiveness on aortic endothelium was observed and analyzed by computer-aided system.Results Compared with the control group,hyperlipidemic rats showed lower level of NO and increase in leukocyte accumulation on the endothelial surface,as well as stronger and more extensive endothelial expression of VCAM-1.In contrast,in fenofibrate-treated group,expression of VCAM-1 as well as leukocyte adhesion significantly decreased which was associated with increased NO level.Conclusion NO activity is inhibited by hypertipidemia which facilitates endothelial impairment of VCAM-1.Fenofibrate can prevent atherosclerosis by restoring NO concentration and down-regulating of VCAM-1 expression.
Key concepts: Fenofibrate, Hyperlipidemia, VCAM-1, Internal medicine, Medicine, Endothelium, Endothelial stem cell, Endocrinology