Martín Fernández, Beatriz

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Martín Fernández
Universidad Complutense de Madrid
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Now showing 1 - 2 of 2
  • Publication
    Low Phytanic Acid-Concentrated DHA Prevents Cognitive Deficit and Regulates Alzheimer Disease Mediators in an ApoE−/− Mice Experimental Model
    (MDPI, 2018) Ruiz-Roso Guerra, María Belén; Echeverry Alzate, Víctor; Ruiz-Roso Calvo de la Mora, Baltasar; Quintela, José; Ballesteros Rodrigálvarez, Sandra; Lahera Julia, Vicente; Heras Jiménez, Natalia de las; López Moreno, José Antonio; Martín Fernández, Beatriz
    Alzheimer’s disease (AD) is the main cause of dementia and cognitive impairment. It has been associated with a significant diminution of omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) levels in the brain. Clinical trials with DHA as a treatment in neurological diseases have shown inconsistent results. Previously, we reported that the presence of phytanic acid (PhA) in standard DHA compositions could be blunting DHA’s beneficial effects. Therefore, we aimed to analyze the effects of a low PhA-concentrated DHA and a standard PhA-concentrated DHA in Apolipoprotein E knockout (ApoE
  • Publication
    Proanthocyanidins Maintain Cardiac Ionic Homeostasis in Aldosterone-Induced Hypertension and Heart Failure
    (MPDI, 2021-09-04) Heras Jiménez, Natalia de las; Galiana, Adrián; Ballesteros Rodrigálvarez, Sandra; Olivares Álvaro, Elena; Fuller, Peter J.; Lahera Julia, Vicente; Martín Fernández, Beatriz
    Excess aldosterone promotes pathological remodeling of the heart and imbalance in cardiac ion homeostasis of sodium, potassium and calcium. Novel treatment with proanthocyanidins in aldosterone-treated rats has resulted in downregulation of cardiac SGK1, the main genomic aldosterone-induced intracellular mediator of ion handling. It therefore follows that proanthocyanidins could be modulating cardiac ion homeostasis in aldosterone-treated rats. Male Wistar rats received aldosterone (1 mg kg−1 day−1) +1% NaCl for three weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5 mg kg−1 day−1). PRO80 prevented cardiac hypertrophy and decreased calcium content. Expression of ion channels (ROMK, NHE1, NKA and NCX1) and calcium transient mediators (CAV1.2, pCaMKII and oxCaMKII) were reduced by PRO80 treatment in aldosterone-treated rats. To conclude, our data indicate that PRO80 may offer an alternative treatment to conventional MR-blockade in the prevention of aldosterone-induced cardiac pathology.