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Relevant bibliographies by topics / Mildronate

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Academic literature on the topic 'Mildronate'

Author: Grafiati

Published: 10 March 2023

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Journal articles on the topic "Mildronate"

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Pupure, Jolanta, Juris Rumaks, Sergejs Isajevs, Olga Korzakova, Jelena Puncule, Simons Svirskis, Ivars Kalviņš, and Vija Kluša. "Mildronate's protective effects in the peripheral nervous system: stavudine-induced neuropathy and formalin-induced inflammation." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 64, no. 3-4 (January 1, 2010): 114–18. http://dx.doi.org/10.2478/v10046-010-0032-7.

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Mildronate's protective effects in the peripheral nervous system: stavudine-induced neuropathy and formalin-induced inflammation Mildronate, previously known as a cardioprotective drug, recently was found to normalise mitochondrial processes by preventing the dysfunction of complex I in rat liver mitochondria. Previously we have shown also the ability of mildronate to prevent pathologies in the central nervous system by normalizing the expression of different signalling molecules in brain tissue. This allowed us to suggest that mildronate may possess a beneficial role also in peripheral nervous system pathologies. The present study was designed to assess the peripheral tissue damage caused by anti-HIV drug stavudine, as well as pain and inflammation caused by formalin. For this demonstration, we investigated the influence of mildronate: (1) on decreased myelin expression and increased neuron degeneration in rat sciatic nerve tissue caused by stavudine; and (2) on formalin-induced inflammation in mice. We found that mildronate protected the stavudine-induced degeneration of neurons in rat peripheral sciatic nerve without a significant influence on demyelination. In a formalin test, mildronate showed anti-inflammatory action comparable to that of indomethacin, a reference drug. The present results show that mildronate is capable of regulating peripheral nerve damage and peripheral inflammatory responses. We suggest that the multifunctional effects of mildronate can be attributed to its ability to regulate mitochondrial processes. The obtained data indicate protective effects of mildronate in different peripheral neurological pathologies.

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Pupure, Jolanta, Sergejs Isajevs, Ivars Kalviņš, and Vija Kluša. "Protective effects of mildronate in indinavir- and efavirenz-induced toxicity in mice." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 64, no. 3-4 (January 1, 2010): 119–24. http://dx.doi.org/10.2478/v10046-010-0025-6.

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Protective effects of mildronate in indinavir- and efavirenz-induced toxicity in mice Previously we showed that mildronate effectively protected mice heart tissue against the toxic influence of anti-HIV drugs azidothymidine, stavudine and lamivudine, which belong to nucleosideanalogue reverse transcriptase inhibitor (NRTI) class. Recently we also demonstrated that mildronate protected isolated rat liver mitochondria against mitochondrial damage caused by azidothymidine. The present study was devoted to examine the possible protective effectiveness of mildronate in cardio-, hepato- and neurotoxicity models caused by anti-HIV drugs of other classes: indinavir, a representative of protease inhibitor (PI) class, and efavirenz, a non-nucleoside-analogue reverse transcriptase inhibitor (NNRTI). Drugs were administered intraperitoneally for two weeks, at the dose of 50 mg/kg of anti-HIV drugs and 100 mg/kg for mildronate. Afterwards, mice heart, liver and brain tissue were examined morphologically and immunohistochemically. The results showed that indinavir in heart tissue caused inflammatory and degenerative changes, manifested as increased expression of nuclear factor kappaBp65 (NF-kBp65), as well as cardiomyocyte necrosis and cellular infiltration. Efavirenz did not cause pathological changes in mice heart tissue, whereas it induced marked expression of caspase-3 and glial fibrillary acidic protein (GFAP) in mice brain tissue and small degenerative alterations in mice liver tissue. The data obtained show mildronate's protective properties in indinavir-induced cardiotoxicity and efavirenz-induced neurotoxicity.

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Prous, J., and J. Castañer. "MILDRONATE." Drugs of the Future 14, no. 1 (1989): 29. http://dx.doi.org/10.1358/dof.1989.014.01.76485.

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4

Gordeev, I. G., and E. O. Taratukhin. ""TREAT THE PATIENT, RATHER THAN THE DISEASE": MILDRONATE AS A COMPONENT OF COMPLEX CARDIOVASCULAR THERAPY." Cardiovascular Therapy and Prevention 12, no. 3 (June 20, 2013): 95–98. http://dx.doi.org/10.15829/1728-8800-2013-3-95-98.

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The paper focuses on cytoprotective and additional effects of mildronate. The emphasis is on the latest original research evidence on mildronate effects in the settings of cardiovascular and cerebral ischemia. The authors also describe the latest laboratory data on the new therapeutic potential of mildronate.

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5

Dzerve, Vilnis. "A Dose-Dependent Improvement in Exercise Tolerance in Patients With Stable Angina Treated With Mildronate: A Clinical Trial “MILSS I”." Medicina 47, no. 10 (November 5, 2011): 78. http://dx.doi.org/10.3390/medicina47100078.

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Objective. To assess the efficacy of various doses of Mildronate in combination with standard therapy for the exercise tolerance of patients with stable angina pectoris. The primary efficacy variable was the change in exercise time in bicycle ergometry from the baseline to 12 weeks of treatment. The secondary endpoints were the changes in maximum achieved load and time to the onset of angina from the baseline to week 12. Material and Methods. A total of 512 patients with chronic coronary heart disease who had ischemia as the limiting factor in the exercise test from 72 study centers in 4 countries were enrolled in this prospective, randomized, double-blind, placebo controlled phase 2 study. The patients were assigned to either 4 groups receiving standard therapy plus Mildronate at different daily doses or 1 group receiving standard therapy plus placebo. Results. The mean change in the total exercise time in the mildronate 100 mg and mildronate 300 mg groups was –2.12±108.45 and 11.48±62.03 seconds, respectively. The mean change for the placebo group was –7.10±81.78 seconds. The difference between Mildronate 100 mg and 300 mg and placebo groups was not significant. Patients in the Mildronate 1000 mg group showed a remarkable increase in the mean change in the total exercise time (35.18±53.29 seconds, P=0.002). Mildronate at a dose of 3000 mg caused a smaller increase as compared with a dose of 1000 mg. Similar changes in the secondary end parameters were observed. Conclusion. The most effective dose of Mildronate in combination with standard therapy was found to be 500 mg twice a day.

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Isajevs, Sergejs, Darja Isajeva, Ulrika Beitnere, Baiba Jansone, Ivars Kalvinsh, and Vija Klusa. "Mildronate as a Regulator of Protein Expression in a Rat Model of Parkinson’s Disease." Medicina 47, no. 10 (November 5, 2011): 79. http://dx.doi.org/10.3390/medicina47100079.

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Background. Mildronate (3-[2,2,2-trimethylhydrazinium] propionate dihydrate) traditionally is a well-known cardioprotective drug. However, our recent studies convincingly demonstrated its neuroprotective properties. The aim of the present study was to evaluate the influence of mildronate on the expression of proteins that are involved in the differentiation and survival of the nigrostriatal dopaminergic neurons in the rat model of Parkinson’s disease (PD). The following biomarkers were used: heat shock protein 70 (Hsp70, a molecular chaperone), glial cell line-derived nerve growth factor (GDNF, a growth factor promoting neuronal differentiation, regeneration, and survival), and neural cell adhesion molecule (NCAM). Material and Methods. PD was modeled by 6-hydroxydopamine (6-OHDA) unilateral intrastriatal injection in rats. Mildronate was administered at doses of 10, 20, and 50 mg/kg for 2 weeks intraperitoneally before 6-OHDA injection. Rat brains were dissected on day 28 after discontinuation of mildronate injections. The expression of biomarkers was assessed immunohistochemically and by Western blot assay. Results. 6-OHDA decreased the expression of Hsp70 and GDNF in the lesioned striatum and substantia nigra, whereas in mildronate-pretreated (20 and 50 mg/kg) rats, the expression of Hsp70 and GDNF was close to the control group values. NCAM expression also was decreased by 6-OHDA in the striatum and it was totally protected by mildronate at a dose of 50 mg/kg. In contrast, in the substantia nigra, 6-OHDA increased the expression of NCAM, while mildronate pretreatment (20 and 50 mg/kg) reversed the 6-OHDA-induced overexpression of NCAM close to the control values. Conclusion. The obtained data showed that mildronate was capable to regulate the expression of proteins that play a role in the homeostasis of neuro-glial processes.

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Sokolovska, J., J. Rumaks, N. Karajeva, D. Grinvalde, J. Sharipova, V. Klusha, I. Kalvinsh, and N. Sjakste. "The influence of mildronate on peripheral neuropathy and some characteristics of glucose and lipid metabolism in rat streptozotocin-induced diabetes mellitus model." Biomeditsinskaya Khimiya 57, no. 5 (2011): 490–500. http://dx.doi.org/10.18097/pbmc20115705490.

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Streptozotocin (STZ) was used to induce the diabetic rat model. STZ rats were treated with mildronate (100 mg/kg daily, per os or intraperitoneally for 6 weeks). Body weight, blood glucose, triglyceride, ketone body concentrations, glycated hemoglobin percent (HbA1c%), glucose tolerance, and the development of neuropathic pain were monitored throughout the experiment. In the STZ + mildronate group, mildronate treatment caused a significant decrease in mean blood glucose (on week 4) and triglyceride concentrations (on weeks 3-6), significantly slowed the increase in HbA1c% (on week 6) and improved glucose tolerance 120 minutes after glucose ingestion during oral glucose tolerance test versus the STZ group. Mildronate completely protected development of STZ-induced neuropathic pain from the first administration week up to end of the experiment. The obtained data indicate clinical usefulness of the drug for the treatment of diabetes mellitus and its complications.

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Mikhin, V. P., Yu M. Pozdnyakov, F. E. Khlebodarov, and O. N. Koltsova. "Mildronate in cardiology practice – current evidence, ongoing research, and future perspectives." Cardiovascular Therapy and Prevention 11, no. 1 (February 20, 2012): 96–103. http://dx.doi.org/10.15829/1728-8800-2012-1-96-103.

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The review discusses the benefits and various practical aspects of the new cardioprotector mildronate use in cardiology. The latest evidence on the mildronate role in complex therapy of patients with stable angina, or patients in the rehabilitation period after myocardial infarction, is summarised.

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Tolstov, S. N., and V. B. Mychka. "Metabolic (cytoprotective) therapy of menopausal disturbances." Cardiovascular Therapy and Prevention 10, no. 3 (June 20, 2011): 72–75. http://dx.doi.org/10.15829/1728-8800-2011-3-72-75.

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The paper presents modern views on cardiovascular aspects of menopause and metabolic therapy of menopausal disturbances with meldonium (Mildronate®). The role of estrogen deficiency in climacteric disturbance development, key pathogenetic mechanisms of menopausal metabolic syndrome (MS), and relevant features of arterial hypertension and endothelial dysfunction development are discussed. The data on Mildronate® clinical use for cardiovascular prevention are summarized. The wide prevalence and multiple clinical manifestations of menopausal disturbances point to the need for their complex therapy. Mildronate® therapy is a new approach for systemic correction of metabolic disturbances in women with climacteric symptoms and menopausal MS.

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Tolstov, S. N., V. B. Mychka, I. A. Salov, Yu V. Prokhorova, and V. A. Vyshivanyuk. "Comparative effectiveness of the approaches to correct vascular structural and functional disturbances in postmenopausal women." Cardiovascular Therapy and Prevention 11, no. 4 (August 20, 2012): 23–35. http://dx.doi.org/10.15829/1728-8800-2012-4-23-35.

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Aim.To compare the effects of Mildronate and hormone replacement therapy (HRT) with estradiol (1 mg) and drospirenone, DSPR (2 mg) on circadian blood pressure (BP) profile, arterial structure and function, and vascular stiffness parameters in women with early postmenopause and climacteric syndrome (CS).Material and methods.The study included 94 women with early postmenopause and CS, who provided written informed consent to participate and were divided into two groups. Group I included 36 women receiving Mildronate (500 mg twice a day), while Group II included 28 women who were administered, according to clinical indications, HRT (1 mg 17β-estradiol and 2 mg DRSP once a day). The control group (CG) included 30 women who did not receive either Mildronate or DRSP. At baseline and 16 weeks later, all participants underwent the assessment of blood biochemistry; intima-media thickness (IMT) of common carotid artery (CCA); endothelium-dependent vasodilatation (EDVD) of brachial artery (BA); antithrombogenic activity of vascular wall; aortal pulse wave velocity (aPWV); arterial stiffness; and 24-hour BP monitoring (BPM).Results.The study demonstrated positive effects of Mildronate therapy and HRT (1 mg 17β-estradiol and 2 mg DRSP) on metabolic status, circadian dynamics and variability (Var) of BP, and arterial structure and function. The largest positive changes in blood lipid profile were observed in Group I and II patients. By the end of the study, these patients demonstrated significantly decreased levels of systolic and diastolic BP and reduced BP Var, particularly in Group II. Mildronate therapy, but not HRT, was associated with normalisation of vascular wall antiaggregant potential. Group II demonstrated a significant reduction in CCA IMT levels, with a similar tendency in Group I. In both groups, the degree of endothelial dysfunction (ED) decreased, which was manifested in increased BA EDVD, decreased aPWV, and reduced arterial stiffness and was more pronounced in Group II.Conclusion.In menopausal women with CS, the effects of Mildronate and HRT on metabolic, structural, and functional disturbances were similar. Therefore, Mildronate therapy could be a new method of correction of these systemic disturbances.

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Dissertations / Theses on the topic "Mildronate"

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Di, Cristo Francesca. "Design, synthesis, biological studies of new mitochondrial modulators improving neurological deficits in experimental models of Huntington's disease." Doctoral thesis, Universita degli studi di Salerno, 2017. http://hdl.handle.net/10556/2488.

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Хабаль, О. В., and А. П. Симончук. "Ефективність мілдронату у хворих із хронічною серцевою недостатністю." Thesis, Сумський державний університет, 2017. http://essuir.sumdu.edu.ua/handle/123456789/54941.

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Хронічна серцева недостатність(ХСН) це кінцева стадія багатьох захворювань серця. Повноцінна і адекватна терапія ХСН дозволяє зменшити вираженість клінічних проявів та покращити прогноз для життя пацієнта.

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Conference papers on the topic "Mildronate"

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Dzhandarova, T. I., M. O. Tabunshchikova, A. S. Rechitsky, A. M. Dadaev, R. J. Kasumova, T. A. Umkhanova, A. V. Alyapkina, O. M. Plahutina, and K. Saakyan. "Comparative assessment of the influence of propolis and mildronate on the dynamics of aldosterone and electrolytes in the blood during the development of chronic heart failure during the periods of the first and second ontogenesis maturity." In II Международная конференция, посвящеенная 100- летию И.А. Држевецкой. СКФУ, 2022. http://dx.doi.org/10.38006/9612-62-6.2022.145.148.

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