This study reveals GLAS reduces platelet aggregation and lipid peroxidation in rats with myocarditis, implying potential cardiovascular benefits.
This study investigated the effects of GLAS, a supramolecular complex composed of the monoammonium salt of glycyrrhizic acid and aspirin, on vascular-platelet hemostasis, lipid peroxidation (LPO), mitochondrial function, respiratory chain enzyme activity, and the NO-ergic system in an experimental model of adrenaline-induced myocarditis. In vitro, GLAS and aspirin at concentrations of 10⁻² and 10⁻³ mg/mL significantly reduced ADP-induced platelet aggregation by 2-3 times for aspirin and 2-5 times for GLAS. In vivo, GLAS transiently reduced platelet count and decreased adhesion by 42% and aggregation by 46%. Myocarditis led to a 98% increase in malondialdehyde (MDA), a key marker of LPO, while GLAS reduced MDA levels by 68% in myocardial cell homogenates and by 62.2% in cardiac mitochondria. Additionally, myocarditis impaired oxidative phosphorylation, reduced mitochondrial respiration, and inhibited succinate dehydrogenase and NAD dehydrogenase by 47.6% and 40.7%, respectively. GLAS and aspirin improved mitochondrial function, with GLAS showing greater efficacy in enhancing oxidative phosphorylation and stimulating enzyme activity. Moreover, myocarditis increased nitric oxide metabolite levels due to elevated inducible nitric oxide synthase (iNOS) activity, and GLAS more effectively reduced iNOS expression than aspirin, although it did not fully normalize the parameters. These findings suggest that GLAS, through its pronounced antioxidant and anti-inflammatory effects, offers protective benefits to cardiac muscle cells in myocarditis and may serve as a promising therapeutic agent for cardiovascular complications associated with this condition.
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A 2025 study studied this question.
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