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Cardiovascular Changes Related to Metabolic Syndrome: Evidence in Obese Zucker RatsMartinelli, Ilenia, Tomassoni, Daniele, Moruzzi, Michele, Roy, Proshanta, Cifani, Carlo, Amenta, Francesco, Tayebati, Seyed Khosrow 11 January 2024 (has links)
Metabolic syndrome (MetS) is a predictor of cardiovascular diseases, commonly
associated with oxidative stress and inflammation. However, the pathogenic mechanisms
are not yet fully elucidated. The aim of the study is to evaluate the oxidative status and
inflammation in the heart of obese Zucker rats (OZRs) and lean Zucker rats (LZRs) at different
ages. Morphological and morphometric analyses were performed in the heart. To study the
oxidative status, the malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), protein oxidation,
and antioxidant enzymes were measured in plasma and heart. To elucidate the inflammatory
markers involved, immunohistochemistry and Western blot were performed for cellular adhesion
molecules and proinflammatory cytokines. OZRs were characterized by hypertension, hyperlipidemia,
hyperglycemia, and insulin resistance. The obesity increased MDA and decreased the activities
of superoxide dismutase (SOD) in plasma as well as in the heart, associated with cardiomyocytes
hypertrophy. OxyBlot in plasma and in heart showed an increase of oxidativestate proteins in OZRs.
Vascular cell adhesion molecule-1, interleukin-6, and tumor necrosis factor-α expressions in OZRs
were higher than those of LZRs. However, these processes did not induce apoptosis or necrosis of
cardiomyocytes. Thus, MetS induces the lipid peroxidation and decreased antioxidant defense that
leads to heart tissue changes and coronary inflammation
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Potentiel de la formulation EPA/DHA 6/1 à prévenir la dysfonction endothéliale et le remodelage cardiopulmonaire dans l’hypertension artérielle pulmonaire chez le rat / Potential of the EPA/DHA 6/1 formulation to prevent endothelial dysfunction and cardiopulmonary remodeling in pulmonary arterial hypertension in ratsAmissi, Said 19 September 2016 (has links)
L’hypertension artérielle pulmonaire (HTAP) est une pathologie affectant les artères pulmonaires de petit calibre entraînant une augmentation des résistances artérielles pulmonaires aboutissant à une défaillance cardiaque droite. La vasoconstriction, le remodelage des artères pulmonaires distales, l’inflammation et le stress oxydant sont de facteurs clés de la pathogénèse de l'HTAP. Nous avons testé les potentiels de la formulation EPA:DHA 6:1 à prévenir l’hypertension pulmonaire et les altérations cardiovasculaires et pulmonaires induites par l’injection de monocrotaline chez le rat. Le traitement des rats monocrotaline avec l’EPA:DHA 6:1 (500 mg/kg/j, p.o) prévient significativement l’élévation de la pression artérielle pulmonaire moyenne, la pression systolique du ventricule droit, diminue le débit cardiaque, l’hypertrophie et la dilatation du ventricule droit. L’EPA:DHA 6:1 réduit également les résistances vasculaires pulmonaires, le remodelage des artérioles pulmonaires et les infiltrations lymphocytaires et macrophagiques. De plus, l’EPA:DHA 6:1 inhibe la production des espèces réactives de l’oxygène, diminue la surexpression des sous-unités p22phox et p47phox de la NADPH oxydase, des cyclooxygénases 1 et 2, des récepteurs ETA et ETB de l’endothéline-1, de la eNOS découplée et améliore la dysfonction endothéliale des artères pulmonaires. L’EPA:DHA 6:1 exercent des effets anti-inflammatoires, antioxydants et vasoprotecteurs et prévient le développement de l’HTAP induite par l’injection de monocrotaline chez le rat. / Pulmonary arterial hypertension (PAH) is characterized by remodeling of the small pulmonary arteries leading to a progressive increase in pulmonary vascular resistance and right ventricular failure. Pulmonary endothelial dysfunction, inflammation and oxidative stress promote the development of pulmonary hypertension. Omega-3 polyunsaturated fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acids (DHA) have been shown to protect the cardiovascular system and reduce inflammation and oxidative stress. The present study evaluate the potential of EPA:DHA 6:1 to prevent monocrotaline-induced PAH in rats. EPA:DHA 6:1 treatment (500 mg/kg/d, p.o) prevented the MCT-induced mean pulmonary arterial pressure, right ventricular systolic pressure and decreased cardiac output. EPA:DHA 6:1 also attenuated right ventricular hypertrophy by reducing Fulton’s index and pulmonary arterial remodeling, decreased lymphocytes T and macrophages infiltration. EPA:DHA 6:1 treatment significantly reduced MCT-induced vascular oxidative stress and improved endothelial function in pulmonary arteries. The protective effect of EPA:DHA 6:1 was associated with the prevention of the MCT-induced upregulation of NADPH oxidase subunits (p22phox and p47phox), COX-1 and COX-2, endothelin A and B receptors and uncoupled eNOS in pulmonary arterioles. Our studies show that the EPA:DHA 6:1 formulation exerts anti-inflammatory, anti-oxidant and has a protective vascular effect in the pulmonary arteries, which may contribute to prevent and potentially cure pulmonary hypertension induced by MCT in rat.
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