[PS 04-02] EFFECTS OF AN ELASTIN PEPTIDE DERIVED FROM THE BULBUS ARTERIOSUS OF BONITOS ON THE OCCURRENCE OF VASCULAR DAMAGE IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS.

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Abstract

Objective:

Elastic fiber, mainly composed by elastin, is an essential structural component of arterial wall and contribute to blood circulation by its elastic property, thus degenerative/destructive changes in elastic fibers cause circulatory disturbance. On the other hand, it has been reported that elastin peptides have diverse biologic roles, including proliferative, chemoattractant and vasorelaxant effects. This study aimed to determine the effects of an elastin peptide derived from the bulbus arteriosus of bonitos on vascular dysfunction in stroke-prone spontaneously hypertensive rats (SHRSPs).

Design and Method:

Male 15-week-old SHRSP/KPO rats were fed without (control group) or with elastin peptide twice a day at a dose of 600 mg/kg body weight /day for 4 weeks (elastin group). At the end of experiment, histological findings associated with hypertensive nephropathy were observed by light microscopy. Furthermore, using thoracic aortas, we assessed endothelial changes by scanning electron microscopy. Vascular reactivity (contraction and relaxation) and pressure-induced distension were also compared. mRNA levels of endothelial nitric oxide synthase (eNOS) and intercellular adhesion molecule-1 (ICAM-1) were investigated by real-time-polymerase chain reaction.

Results:

No significant differences were found in blood pressure and vascular reactivity between the control and elastin groups. The incidence of hypertensive arterial changes such as fibrinoid necrosis, or onion-skin-lesion in renal cortex were lower in the elastin group (p < 0.05). Furthermore, the aortas of the elastin group displayed limited endothelial damage compared with those in the control group. ICAM-1 mRNA levels were suppressed in the elastin group, but eNOS levels remained unchanged between groups.

Conclusions:

In this study, the elastin peptide partially suppressed hypertensive vascular injuries, although it did not delay the occurrence of severe hypertension in SHRSP. Further studies are required to identify the most effective peptide sequence and determine the underlying mechanisms, such as the elastin receptor involved.

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