Abstract

This study aimed to evaluate the protective role of ground raspberry seeds (RBS) as a source of polyphenols and essential fatty acids on blood plasma enzymatic antioxidant status, lipid profile, and endothelium-intact vasodilation during physiological and pathological conditions. Young normotensive Wistar–Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) at ten weeks of age were fed with either a control diet or were supplemented with added 7% RBS for six weeks (n = 6). The main component of RBS was dietary fiber (64%) and the main polyphenols were ellagitannins (1.2%) and flavan-3-ols (0.45%). Irrespective of the rat model, ground RBS decreased liver enzyme aspartate aminotransferase (0.9-fold) and hydrogen peroxide scavenging capacity (Catalase, 0.9-fold). In supplemented SHRs, preincubation with inducible nitric oxide synthase (iNOS) inhibitor 1400W, nonselective cyclooxygenase (COX) inhibitor indomethacin, selective COX-2 inhibitor NS-398, prostacyclin (PGI2) synthesis inhibitor tranylcypromine (TCP), thromboxane receptor (TP) antagonist SQ-29548, thromboxane synthesis inhibitor furegrelate, and 20-HETE synthesis inhibitor HET0016 induced the same relaxant response to acetylcholine as in the nonsupplemented control group. In supplemented WKYs, atherogenic index was decreased (0.8-fold), while iNOS and COX-2-derived PGI2 increased acetylcholine-induced vasodilation. These effects of ground RBS may constitute a potential mechanism for preventing cardiovascular diseases.

Highlights

  • Vascular inflammation and increased vascular resistance play a primary role in the pathogenesis and progression of hypertension [1]

  • Raspberry ellagitannins were mainly constituted by a sanguiin-H-6 (40%) and a lambertianin C (31%), see Table 1

  • Our findings revealed that supplemented normotensive rats had a lower risk of obesity and cardiovascular complications compared to nonsupplemented subjects, as indicated by the decreased atherogenic level

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Summary

Introduction

Vascular inflammation and increased vascular resistance play a primary role in the pathogenesis and progression of hypertension [1]. Vascular dysfunction associated with hypertension is characterized by the attenuated endothelium-dependent vasodilation, which suggests reduced bioavailability of nitric oxide (NO) either in response to decreased production or increased utilization. During this process, superoxide (O2 – ), hydrogen peroxide (H2 O2 ), or peroxynitrite (ONOO− ) are formed. Endothelial cells are able to control the tension of arteries through the release of several vasoactive factors, which balance each other out to obtain the physiological response Among these factors vasodilators e.g., NO, H2 O2 , endothelium-derived hyperpolarizing factor (EDHF), prostacyclin as well as vasoconstrictors e.g., 20-hydroxyeicosatetraenoic acid (20-HETE), isoprostanes, and prostaglandins are the most important regulators of vascular tension in arteries [2,3]

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