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- Antihypertensive effect of spent brewer yeast peptidePublication . Amorim, M.; Marques, C.; Pereira, J. O.; Guardão, L.; Martins, M. J.; Osório, H.; Moura, D.; Calhau, C.; Pinheiro, H.; Pintado, M.Numerous studies have investigated dietary approaches to prevent chronic lifestyle-related diseases, including hypertension. Spent brewer's yeast is the second largest byproduct originated by the brewing industry and it deserves considerable attention because of its high nutritional value, ca. 40% of its dry mass is rich in protein which can be hydrolyzed into biologically active peptides. To upgrade this byproduct, the aim of this study was initially in vitro assessment of biological properties, e.g. ACE inhibition and antioxidant activity, and then, the in vivo effect in short-term oral antihypertensive effect of hydrolyzed yeast fractions on a well characterized model to study hypertension - Spontaneously Hypertensive Rats (SHR). Here, it was demonstrated that the fraction with molecular weight below 3 kDa containing tri and tetra- peptides with hydrophobic amino acid residues - SPQW, PWW and RYW, causes the most noticeable decrease in systolic, diastolic and mean blood pressure of SHR and shows highest antioxidant effect. These properties highlight the potential use of yeast extract as nutraceutical or functional food ingredient for the management and treatment of hypertension with antioxidant effect.
- Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged ratPublication . Rocha, B.; Rodrigues, A. R.; Tomada, I.; Martins, M. J.; Guimarães, J. T.; Gouveia, A. M.; Almeida, H.; Neves, D.Background: Endothelial dysfunction underlies cardiovascular disease that frequently affects aged individuals. Characterized by local decrease in nitric oxide, it results from down-regulation of endothelial nitric oxide synthase (eNOS) expression/activity. Aiming to elucidate the molecular mechanisms involved in age-related endothelial dysfunction and to unveil potential therapeutic targets, we tested how diet pattern, exercise and atorvastatin modulate the expression of eNOS, inducible NOS (iNOS), endothelin-1, sirtuins (SIRT) and microRNA-155 in the erectile tissue of high-fat fed aged rats. Methods: Sprague-Dawley male rats fed with high-fat diet until they completed 12 months were grouped and subjected to energy restriction (ER), ER and atorvastatin, or, ER, atorvastatin and physical exercise. Controls were fed with standard rodent chow. The blood pressure was measured using the tail-cuff method before sacrifice at 18 months. Glucose, total cholesterol, HDL, triglyceride and CRP were assessed in blood and eNOS, endothelin-1, iNOS and sirtuins were detected by immunofluorescence in the penis sections; eNOS, endothelin-1, iNOS, SIRT2–4 and SIRT6–7 were semi-quantified by western blotting in tissue homogenates. MicroRNA-155 was quantified using RT-PCR in formalin-fixed paraffin embedded sections. To compare the studied variables, two-tail student t test was used. Results: Atorvastatin promotes eNOS expression and is more efficient than ER or exercise in the control of hyperlipidemia and inflammation. Among the studied sirtuins, detected for the first time in the erectile tissue of the aged rat, SIRT2 aligns with eNOS expression. Both proteins exhibit over-expression in animals with combined exercise, atorvastatin and ER. Analysis of microRNA-155 expression also suggests its intervention in the regulation of eNOS expression. ER, particularly when combined with atorvastatin, was able to reverse the increase of iNOS and endothelin-1 in high-fat fed rats. Conclusions: The present results indicate that the association of ER, atorvastatin and exercise is more efficient than isolated interventions in the prevention of endothelial dysfunction.