Single article

DOI: 10.47026/2413-4864-2023-3-94-101

Pozdnyakov D.I., Vichorʹ A.A., Adjiachmetova S.L.

The Effect of dry White Mistletoe Extract on the Change in the Ratio of Mitochondrial Subpopulations in the Myocardium in Animals with Alcoholic Cardiomyopathy

Keywords: alcoholic cardiomyopathy, alcoholism, cardioprotectors, mitochondria, extract, white mistletoe

The aim of the research was to study the cardioprotective effect of dry white mistletoe extract in the context of assessing its effect on changes in the activity of interfibrillary and subsarcolemmal mitochondrial subpopulations of the myocardium in experimental alcoholic cardiomyopathy. Materials and methods. Alcoholic cardiomyopathy was modeled in female Wistar rats by course administration of ethanol at the rate of 3 g of absolute ethanol per 1 kg of animal body weight. The studied extract of white mistletoe leaves and the comparison drug – Trimetazidine – were administered orally at doses of 100 mg /kg and 35 mg/kg, respectively. Changes in troponin I concentration and serum creatine phosphokinase activity, citrate synthase activity in mitochondrial subpopulations, and the content of apoptosis markers – apoptosis-inducing factor and caspase 3 in myocardial tissue homogenate were determined during the work. Results and their discussion. The analysis of the results revealed that in rats with alcoholic cardiomyopathy, but without treatment, there is an increase in the concentration of troponin I and creatine phosphokinase activity, accompanied by an increase in the intensity of apoptosis reactions and citrate synthase activity of interfibrillary mitochondria. The use of Trimetazidine and the extract under analysis contributed to a decrease in troponin I content by 19.1% (p < 0.05) and 24.4%, respectively, and creatine phosphokinase activity by 19.8% (p < 0.05) and 28.4% (p < 0.05). It was also established that the activity of subsarcolemmal mitochondria in animals treated with Trimetazidine and white mistletoe extract increased by 121.9% (p < 0.05) and 306.3% (p < 0.05) with a decrease in the activity of citrate synthase of interfibrillary mitochondria by 27.6% (p < 0.05) and 41.4% (p < 0.05). It should be noted that administration of the comparative drug and the studied extract to rats resulted in a decrease in cardiomyocytes' apoptosis, expressed in a decrease in the concentration of apoptosis-inducing factor and caspase 3. Conclusions. In conditions of alcoholic cardiomyopathy, the negative interfibrillary phenotype of mitochondria prevails, which can contribute to the development of energy deficiency in the heart muscle, increasing the degree of myocardial damage. Based on the data obtained, it can be assumed that the extract of white mistletoe contains an active substance of cardioprotective activity associated with restoring the energy metabolism and suppression of apoptosis in the myocardium.

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About authors

Pozdnyakov Dmitriy I.
Candidate of Pharmaceutical Sciences, Head of Department of Pharmacology with a course in Clinical Pharmacology, Pyatigorsk Medical and Pharmaceutical Institute, Russia, Pyatigorsk (pozdniackow.dmitry@yandex.ru; ORCID: https://orcid.org/0000-0002-5595-8182)
Vichor’ Anastasia A.
Educational Master of the Department of Pharmacology with a course in Clinical Pharmacology, Pyatigorsk Medical and Pharmaceutical Institute, Russia, Pyatigorsk (nastyavichory@gmail.com; ORCID: https://orcid.org/0009-0006-1092-7901)
Adjiachmetova Similla L.
Candidate of Pharmaceutical Sciences, Associate Professor of the Department of the organic chemistry, Pyatigorsk Medical and Pharmaceutical Institute, Russia, Pyatigorsk (sima503@mail.ru; ORCID: https://orcid.org/0000-0001-9685-1384)

Article link

Pozdnyakov D.I., Vichorʹ A.A., Adjiachmetova S.L. The Effect of dry White Mistletoe Extract on the Change in the Ratio of Mitochondrial Subpopulations in the Myocardium in Animals with Alcoholic Cardiomyopathy [Electronic resource] // Acta medica Eurasica. – 2023. – №3. P. 94-101. – URL: https://acta-medica-eurasica.ru/en/single/2023/3/10/. DOI: 10.47026/2413-4864-2023-3-94-101.