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The current research sought to determine the cardiotoxic consequences of dexamethasone-high-dose in rats, the therapeutic effects of carvedilol, and the role of the u03b11-adrenergic receptor. In the last four groups, Dexamethasone was administered with the medications. Serum troponin I and creatine kinase, and creatine kinase were determined as well as cardiac fatty acid synthesis, Akt, transforming growth factor-u2013myoglobin, and alpha smooth muscle actin. Blocking the u03b11-adrenergic receptor in carvedilol attenuates the cardioprotective effects against dexamethasone-induced cardiotoxicity.
Source link: https://doi.org/10.1007/s00210-022-02285-5
Carvedilol is one of the most effective u03b-blockers for boosting survival after myocardial infarction. However, the reasons by which carvedilol achieves this superior clinical appearance are also vague. Through CRISPR/Cas9's primary and immortalized cells genome-edited; we find that G proteins are responsible for all detectable carvedilol signalling through molecular dynamics simulations; and, using biological, biochemical, and signalling assays with molecular dynamics simulations, we show that G proteins play all detectable carvedilol signaling through a u03b2_2ARs.
Source link: https://doi.org/10.1038/s41467-022-34765-w
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