Endothelial dysfuncton and 2 type diabetes: novel markers for earlier diagnostics

Khripun, Irina; Morgunov, M. N.; Vorobyov, S. V.; Terentiev, Victoria; Kogan, M. I.

doi:10.15829/1728-8800-2016-5-59-63

Cited by 5 publications

(1 citation statement)

References 7 publications

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“…To assess the molecular targets of DOX and CY-induced ED, we investigated the main parameters of ED [24,25], which are widely used in the clinic and available in many diagnostic laboratories of medical facilities. Also, there is a piece of evidence that TMZ modulates the human aortic vascular smooth muscle cell (HASMC) proliferation [26], and our group fi nds it an interesting additional pivotal point of TMZ-induced morphofunctional state of the endothelium normalization.…”

Section:  Discussionmentioning

confidence: 99%

Trimetazidine as a Modifier of Chemotherapy-Induced Endothelium Homeostasis Disturbances

Авагимян¹,

Кактурский²

2022

Кардиология В Беларуси

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Введение. Настоящее исследование направлено на изучение взаимосвязи между эндотелиальной дисфункцией, кардиотоксичностью АС-режима химиотерапии и триметазидином опосредованной вазопротекции.Цель. Изучить вазотоксический потенциал AC-режима химиотерапии наряду с одновременной оценкой вазопротекторного потенциала триметазидина.Материалы и методы. Проведенное исследование характеризуется как фундаментальное, рандомизированное, контролируемое, экспериментальное, in vivo. С целью проведения экспериментальной работы было задействовано 80 инбредных крыс линии Wistar, которые были рандомно разделены на 4 равные группы. Модель эндотелиальной дисфункции была получена с использованием химиотерапевтического коктейля, состоящего из доксорубицина и циклофосфамида. В качестве вероятного стабилизатора функционирования эндотелия был выбран триметазидин. Курсовая дозировка доксорубицина составила 15 мг/кг, циклофосфамида – 150 мг/кг, а триметазидина – 42 мг/кг. Продолжительность эксперимента – 14 дней.Результаты. В рамках настоящего исследования оценены девиации эндотелина-1, оксида азота, а также факторов адгезии VCAM и ICAM, маркер воспаления – С-реактивный белок. Полученные данные показали, что триметазидин модифицировал усиление эндотелиальной дисфункции.Выводы: 1. АС-режим химиотерапии оказывает выраженное эндотелий-дискоординирующее воздействие. 2. Триметазидин обладает значимым вазопротекторным потенциалом. Introduction. Our research was determined to investigate the link between endothelial dysfunction, AC-mode of chemotherapy and trimetazidine-driven vasoprotection.Purpose. To investigate the AC-mode of chemotherapy-induced endothelium dysfunction and rationality of TMZ prescription.Materials and methods. The conducted study is characterized as a fundamental, randomized, controlled, experimental in vivo study. To carry out the experimental work, 80 inbred Wistar rats were involved, which were randomly divided into 4 equal groups. A model of endothelial dysfunction was generated using a direct combination of doxorubicin and cyclophosphamide. Trimetazidine was used as a probable stabilizer of endothelial activity. Course dose of doxorubicin – 15 mg/kg, course dose of cyclophosphamide – 150 mg/kg, course dose of trimetazidine – 42 mg/kg. The duration of the experiment was 14 days.Results. Within the framework of this study, deviations of endothelin-1, nitric oxide, as well as adhesion factors VCAM and ICAM, and an inflammatory marker, C-reactive protein, were evaluated.Conclusions: 1. AC-mode of chemotherapy provide pronounced endothelium discoordinating impact. 2. TMZ has sufficient vasoprotective properties.

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Section:  Discussionmentioning

confidence: 99%

Trimetazidine as a Modifier of Chemotherapy-Induced Endothelium Homeostasis Disturbances

Авагимян¹,

Кактурский²

2022

Кардиология В Беларуси

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Endothelial function status in hypogonadal men

Khripun

Vorobyev

2022

Diabetes mellitus

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Background: Type 2 diabetes mellitus (T2DM) and hypogonadism are mutually aggravating diseases associated with the development and progression of cardiovascular pathology. The status of endothelial function in men with T2DM and hypogonadism hasn’t been studied.Aims: To assess the effect of hypogonadism on endothelial function in men with T2DM.Materials and methods: Patients underwent clinical studies, assessment of carbohydrate and lipid metabolism, the content of sex hormones (total testosterone (T), sex hormones binding globulin, free T, luteinizing hormone) and markers of endothelial function (nitric oxide (NO), endothelial nitric oxide synthase type 3 (eNOS3), endothelin, adhesion molecules ICAM-1, VCAM-1, p- and e-selectins, cadherin), ultrasound examinations of endothelium-dependent vasodilation (EDVD) of the brachial artery (BA) and carotid arteries with an assessment of the thickness of intima-media complex (TIM) were performed.Results: The study included 276 men with T2DM (age 54.0[49;60] years), who were divided into 2 groups: 1–124 patients with hypogonadism; 2–152 eugonadal patients. Reduction of the endothelial vasomotor function was detected in 32.4% of patients in the 2st group and in 55.3% of the 1nd group (χ2=6.1; p=0.01), which was associated with a decrease in EDVD by 29.8 % (p<0.001) and an increase in the time of development of maximal BA vasodilation by 30 seconds in patients with hypogonadism (p<0.001). The TIM of the carotid arteries was 10% more in group 1 compared with group 2 (p=0.03). The level of NO in the 1st group was reduced by 1.6 times (p=0.001), eNOS3–by 1.5 times (p=0.038) compared with the 2nd group. The concentrations of adhesion molecules were higher in group 1 compared to group 2: VCAM-1 by 32.5% (p<0.001), ICAM-1 by 43.5% (p<0.001), p-selectin–by 19.3% (p=0.004), cadherin–6 times (p<0.001).Conclusion: Hypogonadism in men with T2DM is associated with the development of endothelial dysfunction, which manifests in a weakening of the EDVD and a slowdown in its development, as well as disturbances of the secretory activity of endothelium–a decrease in NO synthesis and activation of the adhesion molecules expression, which can be regarded as an universal pathogenetic mechanism of the development of cardiovascular diseases in combination of T deficiency and T2DM.

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Endothelial dysfunction as a pathogenetic factor of sensorineural hearing loss

Noskova,

Khrabrikov

2024

Vestn. otorinolaringol.

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Endothelial dysfuncton and 2 type diabetes: novel markers for earlier diagnostics

Cited by 5 publications

References 7 publications

Trimetazidine as a Modifier of Chemotherapy-Induced Endothelium Homeostasis Disturbances

Trimetazidine as a Modifier of Chemotherapy-Induced Endothelium Homeostasis Disturbances

Endothelial function status in hypogonadal men

Endothelial dysfunction as a pathogenetic factor of sensorineural hearing loss

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