Trimetazidine in conditions other than coronary disease, old drug, new tricks?

Zou, Hai; Ding, Ye; Jin, Qin-Yang; Qian, Lin-Yan; Huang, Dongsheng; Cen, Xue-jiang

doi:10.1016/j.ijcard.2017.02.083

Cited by 17 publications

(13 citation statements)

References 56 publications

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“…Trimetazidine is a well-described antianginal drug, and it has been widely used to treat cardiovascular diseases, such as coronary heart disease, ischemia-reperfusion injury, heart failure and other cardiac diseases (Argaud et al, 2005; Martins et al, 2012; Zhou et al, 2012; Ma et al, 2016; Zhang et al, 2016; Cui et al, 2017; Zou et al, 2017; He C. et al, 2018; Petrovics et al, 2018), by restoring ischemic cardiomyocytes. In basic medical science, a large numbers of studies report that TMZ plays pivotal roles in the regulation of apoptosis, inflammatory response, and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…It has many cardioprotective effects including reducing vascular resistance, increasing coronary and blood circulation, promoting cardiac metabolism and restoring the ability of energy production (Di Napoli and Taccardi, 2009; Tsioufis et al, 2015; Dezsi, 2016). Previous studies have demonstrated that TMZ can be effective in anti-inflammation and anti-oxidation, anti-apoptosis, improving myocardial metabolism and energy production (Martins et al, 2012; Zhou et al, 2012; Zou et al, 2017). Zhang et al (2016) proved that the early administration of TMZ ameliorated diabetic cardiomyopathy by controlling myocardial fibrosis and cardiomyocyte apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Trimetazidine Attenuates Exhaustive Exercise-Induced Myocardial Injury in Rats via Regulation of the Nrf2/NF-κB Signaling Pathway

et al. 2019

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Exhausted exercise has been reported to cause the damage of myocardial structure and function in terms of cardiomyocyte apoptosis, oxidative stress, and energy metabolism disturbance. Trimetazidine (TMZ), as an anti-ischemic agent, has been approved to be effective in promoting myocardial energy metabolism, anti-inflammatory, and anti-oxidation. However, few studies examined the effects of TMZ on myocardial injury induced by exhausted exercise. To investigate whether TMZ could ameliorate the exhaustive exercise-induced myocardial injury and explore the underlying mechanisms, here the rat model of exhaustive exercise was induced by prolonged swimming exercise and TMZ was administrated to rats before exhaustive exercise. According to the results, we demonstrated that exhaustive exercise led to cardiomyocyte damage in rats as evidenced by elevations in cTnI and NT-proBNP levels, and decrease in CX43 expression, which was attenuated by TMZ treatment. Moreover, the administration of TMZ was found to restrain exhaustive exercise-induced oxidative stress damage by increasing GSH level, SOD and GSH-Px activities, and decreasing MDA level. Additionally, TMZ ameliorated myocardial injury by inhibiting apoptosis via reducing Bax/Bcl-2 ratio and down-regulating cleaved caspase-3, cleaved PARP, and cytochrome c levels in the myocardium of rats. Furthermore, we found that TMZ suppressed oxidative stress and cardiomyocyte apoptosis via activation of Nrf2/HO-1 and inactivation of NF-κB signaling pathways. Therefore, our study suggested that TMZ provided cardioprotection in rats after exhaustive exercise, indicating TMZ might served as a potential therapeutic drug for exhaustive exercise-induced myocardial injury.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Trimetazidine Attenuates Exhaustive Exercise-Induced Myocardial Injury in Rats via Regulation of the Nrf2/NF-κB Signaling Pathway

et al. 2019

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“…Все эти особые свойства препарата триметазидин являются весомым аргументом для перспективного его изучения и при других заболеваниях, не связанных с ИБС и ХСН, таких как периферические заболевания артерий, кардиомиопатия неишемического генеза, сепсис, поражения миокарда на фоне химиотерапии, диабетическая миокардиодистрофия и другие, некоторые из которых уже представлены в различных клинических и экспериментальных исследованиях [14].…”

Section: Discussionunclassified

Trimetazidine Influence on Filtration and Tubulointerstitial Function of Kidneys in Ischemic Heart Disease Patients With Chronic Heart Failure and Renal Dysfunction

2018

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Цель. Оценка влияния триметазидина на показатели фильтрационной и тубулоинтерстициальной функций почек у больных стенокардией II-III функционального класса (ФК) на фоне стабильной хронической сердечной недостаточности (ХСН) II-III ФК в сочетании с хронической болезнью почек (ХБП) 3 стадии. Материал и методы. Обследовано 288 больных стабильной стенокардией II-III ФК, среди которых была выделена когорта из 162 (56,3%) больных ХСН II-III ФК. Среди них у 62 (38,3%) пациентов была зарегистрирована ХБП 3 стадии. Все больные ХСН и ХБП 3 стадии были рандомизированы на две равные группы в зависимости от вида медикаментозного вмешательства. Пациентам первой группы к стандартному лечению ХСН и ишемической болезнью сердца (ИБС), был добавлен препарат триметазидин (Предуктал МВ ® , фирмы Servier, Франция) 35 мг 1 раз в день утром, во второй группе пациенты лечились аналогично без применения триметазидина. Длительность лечения составила 6 месяцев. Для оценки функций почек определяли скорость клубочковой фильтрации (СКФ) (CKD-EPIcre), рассчитанную по креатинину сыворотки крови, цистатин С в крови и СКФ (CKD-EPIcys), рассчитанную по цистатину С, cоотношение альбумина к креатинину мочи в разовой порции (UACR), молекулы повреждения канальцев почек (KIM-1) в моче, тканевый ингибитор матриксных протеиназ 1 типа в крови (ТIMP-1). Результаты. Включение в стандартную терапию больных ИБС и ХСН в сочетании с ХБП 3 стадии триметазидина обеспечивает не только улучшение клинического течения заболеваний, увеличение толерантности к физической нагрузке, но и демонстрирует регресс нарушений функции почек по данным динамики снижения цистатина С (p=0,005), увеличения СКФ, рассчитанной по цистатину С (p=0,012), уменьшения UACR (p=0,002), KIM-1 (p<0,001), восстанавливает благоприятный коллагенолиз в интерстиции почек по результатам динамики снижения TIMP-1 (p<0,001). Заключение. Триметазидин проявляет нефропротективный эффект при включении его в терапию больных ИБС и ХСН в сочетании с ХБП 3 стадии. Этот эффект характеризуется улучшением фильтрационной функции, снижением экскреции альбумина с мочой, уменьшением канальцевых нарушений за счет подавления коллагенообразования в интерстиции почек.

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“…Trimetazidine ( 21 ) is an anti-ischemic drug of the piperazine class. Its mechanism of action is diverse, ranging from increasing nitric oxide production, inhibiting cell apoptosis and being an antioxidant, which increases endothelial function [ 53 ]. Apart from being able to pass through the blood-brain barrier, it can reduce the produce of free radicals, due to its antioxidant properties.…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

Old Drugs as New Treatments for Neurodegenerative Diseases

2018

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Neurodegenerative diseases are increasing in number, given that the general global population is becoming older. They manifest themselves through mechanisms that are not fully understood, in many cases, and impair memory, cognition and movement. Currently, no neurodegenerative disease is curable, and the treatments available only manage the symptoms or halt the progression of the disease. Therefore, there is an urgent need for new treatments for this kind of disease, since the World Health Organization has predicted that neurodegenerative diseases affecting motor function will become the second-most prevalent cause of death in the next 20 years. New therapies can come from three main sources: synthesis, natural products, and existing drugs. This last source is known as drug repurposing, which is the most advantageous, since the drug’s pharmacokinetic and pharmacodynamic profiles are already established, and the investment put into this strategy is not as significant as for the classic development of new drugs. There have been several studies on the potential of old drugs for the most relevant neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Multiple Sclerosis and Amyotrophic Lateral Sclerosis.

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Trimetazidine in conditions other than coronary disease, old drug, new tricks?

Cited by 17 publications

References 56 publications

Trimetazidine Attenuates Exhaustive Exercise-Induced Myocardial Injury in Rats via Regulation of the Nrf2/NF-κB Signaling Pathway

Trimetazidine Attenuates Exhaustive Exercise-Induced Myocardial Injury in Rats via Regulation of the Nrf2/NF-κB Signaling Pathway

Trimetazidine Influence on Filtration and Tubulointerstitial Function of Kidneys in Ischemic Heart Disease Patients With Chronic Heart Failure and Renal Dysfunction

Old Drugs as New Treatments for Neurodegenerative Diseases

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