After single and repeated peroral administration of bemitil to rats this drug was found in the liver, brain, kidneys, spleen, heart, skeletal muscles, lungs, adipose tissue, and testicles. After single treatment accumulation of bemitil was most pronounced in the liver. After repeated treatment the decrease in bemitil concentration in the liver was probably associated with increased elimination of the drug from liver tissue due to intensification of its biotransformation. We conclude that bemitil can accumulate in the blood, but not in tissues.
We studied experimental kinetics of ethomerzol (5-ethoxy-2ethylthiobenzimidazole hydrochloride) distribution in the liver, brain, kidneys, spleen, heart, skeletal muscles, lungs, adipose tissue, and testes of rats after its single or course administration. Peculiarities of ethomerzol distribution in various administration regimens were analyzed. Single treatment led to more pronounced accumulation of the drug in the liver. Study of ethomerzol distribution after course treatment revealed organs and tissues accumulating the drug (blood, brain, heart, kidneys, lungs, and adipose tissue).
Comparative study of experimental kinetics of distribution of benzimidazole derivatives (bemithyl, etomerzole, and thietazole) in organs and tissues was carried out after single and course treatment. The drugs intensely passed into organs and tissues from the blood after treatment by all protocols. Specific features of drug distribution were detected; for example, splenic tissue selectively accumulated thietazole during course treatment.
Introduction. According to the analysis of indicators of the hemostasis system in liver pathology, there are multidirectional data in the literature, which may be associated with the examination of patients with varying degrees of severity and etiology of the process. Aim. The aim of the study was to study the indicators of hemostasis and markers of endothelial damage in patients with non-alcoholic steatosis and liver fibrosis of viral etiology. Materials and methods. A total of 64 people were examined. The first group included 32 patients with non-alcoholic liver steatosis on the background of obesity of 1–2 degrees, with an average age of 46.3 ± 4.3 years (12 men and 20 women). The second group consisted of 22 patients with liver fibrosis on the background of chronic hepatitis C (HCV) with an average age of 36.8 ± 4.7 years (12 men and 10 women). The control group included 10 practically healthy individuals with an average age of 38.9 ± 5.3 years without liver pathology. The number of platelets, platelet aggregation with ADP inducers, collagen and ristocetin, functional activity of Willebrand factor (vWF), coagulation hemostasis and fibrinolysis system, and serum concentration of vascular endothelial growth factor (VEGF) were determined. Statistical processing of the obtained data was carried out using the program “Stat2015”. Results. Induced platelet aggregation in steatosis and liver fibrosis significantly decreased with ADP agonists and collagen against the background of a normal platelet count. In both study groups, signs of endothelial damage with a tendency to increase the functional activity of vWF and VEGF hyperproduction were found. An elongation of thrombin time was also recorded, more significantly in patients with steatosis. Conclusion. Patients with non-alcoholic liver steatosis and liver fibrosis on the background of HCV are characterized by disorders in the vascular-platelet (endothelial damage and thrombocytopathy in the form of platelet hypocoagulation) and coagulation (hypocoagulation) links of hemostasis.
ФГБОУ ВО «Пермский Государственный Медицинский Университет имени академика Е.А. Вагнера», г. Пермь, Российская ФедерацияАннотация. Цель исследования: изучить уровень провоспалительных цитокинов фактора некроза опухоли-альфа (ФНО-α) и интерлейкина-6 (ИЛ-6), концентрацию маркера повреждения эндотелия -васкулоэндотелиаль-ного фактора роста (ВЭФР) и оценить взаимосвязь этих параметров с функциональными печеночными пробами у пациентов со стеатозом (СП), фиброзом (ФП) и циррозом печени (ЦП). Материал и методы. Обследовано 30 пациентов со СП, 27 -с хроническим гепатитом С (ФП) и 25 -с ЦП смешанной этиологии (алкоголь+вирус), 10 практически здоровых лиц. В сыворотке крови оценивали ФНО-α, ИЛ-6 и ВЭФР методом иммуноферментного анализа, а также биохимические тесты. Результаты. В исследуемых группах с поражением печени уровни цито-кинов оказались значимо выше, чем в контроле и имели наибольшие значения при ЦП. ВЭФР также значимо повышался при заболеваниях печени. Максимальные концентрации ВЭФР регистрировались при ФП и ЦП в сравнении со СП (p=0,001 и p=0,001 соответственно). При этом провоспалительные цитокины прямо коррелиро-вали с маркерами цитолиза и холестаза и обратно -с альбумином. Заключение. Хронические заболевания пе-чени на стадиях стеатоза, фиброза и цирроза сопровождаются активацией выработки ФНОα, ИЛ-6 и ВЭФР, что способствует прогрессированию поражения печени, подтверждает их участие в патогенезе развития вышеука-занных патологических процессов и позволяет использовать их в качестве дополнительных лабораторных пара-метров оценки морфофункционального состояния печени. Ключевые слова: стеатоз, фиброз, цирроз печени, эндотелий, цитокины.Введение. Болезни печени являются одной из наиболее актуальных проблем мирового здраво-охранения. Это связано не только с их широкой распространенностью и продолжающимся ростом, но и с высоким уровнем летальных исходов. Бо-лезни печени входят в 10 ведущих причин смерти в странах со средне-низким и средне-высоким уров-нем дохода. Если в 2013 году общая смертность от гепатитов B и C, а также от связанного с ними цир-роза печени (ЦП) составляла 950 тысяч человек в год, то 2015 году этот показатель увеличился до 1 миллиона 480 тысяч человек в год [1].Среди научных публикаций последнего вре-мени встречаются работы, посвященные исследо-ванию провоспалительных цитокинов [2,3] и эндо-телиальной дисфункции [4] при заболеваниях пе-чени. Установлено, что гиперпродукция фактора некроза опухоли-альфа (ФНО-α) и интерлейкина-6 (ИЛ-6), возникающая при ЦП, приводит к более тя-желому повреждению печени и прямо коррелирует с классом цирроза по Chald-Pugh [3]. В то же время доказано, что концентрация вышеназванных цито-кинов значимо повышается у пациентов как со сте-атозом, так и с фиброзом печени и так же имеет прямую связь с тяжестью поражения [5,6].Повреждение эндотелия, проявляющееся гипер-продукцией васкулоэндотелиального фактора ро-ста (ВЭФР) приводит к образованию дополнитель-ных сосудов (капилляризация синусоидов) в пе-чени на фоне воспаления и прогрессированию фиб-роза. По отдельным данным ...
The aim. To study the hepatoprotective effect of the aqueous extract of the leaves of Gynura Procumbens (GP) on an experimental model of fructose-induced non-alcoholic liver steatosis in laboratory animals. Materials and methods. The experimental study was conducted for 30 days on 25 non-inbred sexually mature white male rats aged 8-9 months, weighing 400-530 g., which comprised 3 groups: “Control” (received a full-fledged balanced standard granular feed), “fructose-induced steatosis” (feeding was carried out similarly to animals of the first group using a 15% solution of fructose as drinking water) and “Steatosis + GP” (simulated liver steatosis and simultaneously daily intragastric daily administration of GP leaf extract was performed. Laboratory parameters (transaminases, glucose and lipid spectrum) in blood serum, biometric indicators (animal mass, liver mass and mass coefficient) and histological examination of the liver were studied in all animals according to the conclusion from the experiment. Results. The course of fructose-induced liver steatosis in experimental animals is accompanied by lipid spectrum disorders, hepatomegaly without the formation of general obesity and morphological changes in liver tissue in the form of fatty degeneration without signs of inflammation and fibrosis. Conclusion: The course intragastric administration of an aqueous extract of GP leaves to experimental animals with steatosis does not significantly affect the lipid spectrum, but prevents the formation of hepatomegaly and morphological changes characteristic of steatosis in liver tissue.
We studied the kinetics of thietazole distribution in the liver, brain, kidneys, spleen, heart, skeletal muscles, lungs, adipose tissue, and testicles after single and repeated administration of this drug. Single and repeated administration of thietazole was followed by elimination of this drug from the blood into organs and tissues. After repeated administration, thietazole was selectively accumulated in the spleen.
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