Protective action of N-stearoylethanolamine on blood coagulation and arterial changes in spontaneously hypertensive rats fed cholesterol-rich diet

Abstract

In this work we aimed to test the atherosclerotic changes in the aortic wall and pro-coagulant response of the blood coagulation system of spontaneously hypertensive rats (Shr) fed cholesterol-rich diet (CRD) and to study the effect of the anti-inflammatory agent N-stearoylethanolamine (NSE) on the development of atherosclerosis in this model. Female rats (n = 30) with genetically determined hypertension proven by direct measurement of blood pressure were fed crd (5% cholesterol) for 2 months. control group of Shr (n = 10) received standard pellet diet, 10 were fed crd and 10 received crd with daily per os application of NSe at a dose of 50 mg/kg of body weight. histological analysis detected swelling and detachment of endothelial cells, huge edema of the subendothelial layer and a disruption of the middle shell integrity. crd rats had higher fibrinogen concentration, increased rate of platelet aggregation and decreased level of anticoagulant Pc. Platelet aggregation speed increased in crd-fed rats (52.5±4.1%/min) was slightly normalized under the action of NSe (40±8.3 vs 35±9%/min in controls). Fibrinogen concentration was slightly increased in crdfed rats (2.75±0.7 vs 1.9±0.5 mg/ml in controls). however, the level of anticoagulant Pc that was decreased in crd-fed rats (65±16 vs 100±11% in controls) was normalized under the action of NSe (92±17%). NSe also influenced the aorta architecture, however normalizing the thickness of the aorticwall did not change the cholesterol-induced inclusions within aorta media. NSE anti-inflammatory action changes the atherogenic processes in CRD-fed rats mainly protecting PC from consumption during the inflammatory process and reducing edema of the aorta. however hematological parameters (including clotting time in the aPTT test and fibrinogen concentration) changed independently on NSE application. Anti-aggregatory action of NSE on platelets can be a result of direct action on platelets or the consequence of its anti-inflammatory action. During atherogenesis induced by CRD in the model, NSE demonstrated valuable anti-inflammatory action protecting the organism during atherogenesis, however it cannot be assumed as an antithrombotic or antiatherogenic agent because it is unable to influence hemostasis directly.