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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012441PMC
http://dx.doi.org/10.1093/cvr/cvae266DOI Listing

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Here, we, for the first time, compared the cardioprotective effects of third-generation vasodilating beta-blocker nebivolol (Neb) and conventional beta-blocker metoprolol (Met) on LPS-induced injury in H9c2 cardiomyoblasts. Our findings denoted that Neb and Met pretreatment diminish LPS-mediated cytotoxicity and oxidative stress. Concomitantly, LPS-triggered inflammatory cytokines activation was significantly suppressed by Neb but not by Met.

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Nebivolol in oral subacute treatment prevents cardiac post-ischemic dysfunction in rats, but hyperthyroidism reduces this protection: mechanisms involved.

Naunyn Schmiedebergs Arch Pharmacol

May 2024

Cátedra de Farmacología, Grupo de Farmacología Experimental y Energética Cardíaca (GFEYEC), Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas, Universidad Nacional de La Plata (UNLP), 47 y 115 (1900) La Plata, La Plata, Argentina.

Nebivolol could prevent dysfunction in patients suffering myocardial ischemia. However, influence of hyperthyroidism is not known. Consequences and mechanisms of nebivolol treatment were investigated in isolated hearts from euthyroid (EuT) and hyperthyroid (HpT) rats.

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Article Synopsis
  • The study is about a type of chemotherapy drug called anthracyclines, which can hurt the heart, and it tests a heart-protecting medicine called nebivolol to see if it can prevent this damage.
  • It involves patients with breast cancer or a specific type of lymphoma who have healthy hearts and are starting treatment with anthracyclines.
  • The trial will compare nebivolol to a placebo (like a fake medicine) over a year to see if it helps protect the heart better than not taking it.
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Background: Cancer patients receiving chemotherapy have an increased risk of cardiovascular complications. This limits the widespread use of lifesaving therapies, often necessitating alternate lower efficacy regimens, or precluding chemotherapy entirely. Prior studies have suggested that using common cardioprotective agents may attenuate chemotherapy-induced cardiotoxicity.

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