1 аннотация введение. Несмотря на имеющиеся данные о функционировании опухолевых клеток в условиях свободнорадикального окисления, остается открытым вопрос о механизмах редокс-регуляции, управления пролиферацией клеток и «ускользания» от апоптотической гибели. Цель исследования-выявить участие системы тиоредоксина в регуляции пролиферации клеток аденокарциномы молочной железы линии МСF-7 при модуляции редокс-статуса блокатором SH-групп белков и пептидов N-этилмалеимидом и протектором тиоловых групп-1,4-дитиоэритритолом. Материал и методы. Исследования были выполнены с использованием опухолевой клеточной линии МСF-7, культивируемой адгезионным методом. Редокс-статус клеток модулировали с помощью 5 мМ N-этилмалеимида, блокатора SH-групп белков и пептидов, и 5 мМ 1,4-дитиоэритритола, протектора тиоловых групп. Оценку содержания активных форм кислорода и клеточного цикла проводили методом проточной цитофлуориметрии. Концентрацию восстановленного окисленного глутатиона и активность тиоредоксинредуктазы определяли спектрофотометрическим методом. Внутриклеточное содержание тиоредоксина, циклина Е и циклинзависимой киназы 2 определяли методом вестерн-блоттинга. результаты. Показана важная роль системы тиоредоксина в регуляции пролиферации клеток линии МСF-7. Остановка клеточного цикла в S фазе при действии N-этилмалеимида и в G 0 /G 1 фазе при действии 1,4-дитиоэритритола связана с изменениями активности редокс-чувствительных белковых комплексов, регулирующих пролиферацию (циклинов и циклинзависимых киназ). Заключение. Редокс-зависимая модуляция функционирования внутриклеточных белков, регулирующих пролиферацию, осуществляется при участии системы тиоредоксина. Данное направление исследований представляется перспективным для поиска молекулярных мишеней опухолевой трансформации клеток молочной железы. ключевые слова: окислительный стресс; редокс-статус клеток; тиоредоксин; аденокарцинома молочной железы; пролиферация.
Currently, diabetes ranks third in relation to medical and social significance after cardiovascular diseases and cancer and is the leading cause of blindness; it greatly increases the risk of myocardial infarction, coronary heart disease, nephropathy and hypertension in patients with this disorder; therefore clinical and experimental studies aimed at investigation of diabetes emergence and development mechanisms are urgent.The aim of the study was to investigate the status of oxidative modification of proteins and glutathionedependent antioxidant defense system in adipocytes of rats with alloxan diabetes under conditions of oxidative stress.Material and methods. Development of type 1 diabetes was induced in rats by alloxan administration (90 mg/kg of body mass). Adipocytes were obtained from epididymal adipose tissue of rats. The level of carbonyl derivatives of proteins, oxidized tryptophan, bityrosine, general, reduced, oxygenated and protein-bound glutathione, as well as glutathione peroxidase activity in adipocytes of rats was determined.Results. In adipocytes of rats with alloxan diabetes, concentration of carbonyl derivatives of proteins, bityrosine and oxidized tryptophan increased on the background of redox-potential of glutathione system and glutathione peroxidase activity decrease.Conclusion. The obtained data indicate the activation of free-radical oxidation of proteins and reduction of antioxidant defense under conditions of oxidative stress in the adipose tissue of rats with alloxan diabetes; this process plays an important role in pathogenesis of diabetes and its complications development.
ДИСБАЛАНС ИММУНОРЕГУЛЯТОРНЫХ Th1-И Th2-ЦИТОКИНОВ ПРИ ПЕРСИСТЕНТНЫХ ВИРУСНЫХ ИНФЕКЦИЯХ Наследникова И.О., Рязанцева Н.В., Новицкий В.В., Ткаченко С.Б., Зима А.П. ГОУ ВПО «Сибирский государственный медицинский университетФедерального агентства по здравоохранению и социальному развитию», кафедра патофизиологии и кафедра фундаментальных основ клинической медицины, г. Томск, Резюме. С привлечением современных иммунологических методов исследования освещены некоторые аспекты иммунопатогенеза персистентных вирусных инфекций. Установлено, что длительная персистенция вирусов гепатита В и С, клещевого энцефалита и простого герпеса сопровождается дефектом Т-клеточного звена иммунитета и выраженным дисбалансом продукции мононуклеарными лейкоцитами периферической крови иммунорегуляторных цитокинов преимущественно в направлении Th2.Ключевые слова: Th1-лимфоциты, Th2-лимфоциты, цитокины, вирусные инфекции. Naslednikova I.O., Ryazantseva N.V., Novitsky V.V., Tkachenko S.B., Zima A.P. IMBALANCE OF IMMUNOREGULATORY Th1-AND Th2-CYTOKINES IN PERSISTENT VIRAL INFECTIONSAbstract. The article is considering certain features of immunopathogenesis exhibited in persistent viral infections, taking into account modern data and recently introduced immunological techniques. It has been revealed that a long-term persistence of hepatitis B and C viruses, tick-borne encephalitis, and herpes simplex is accompanied by deficient functioning in the T-cell compartment of immune system, and by markedly altered production of immunoregulatory cytokines in peripheral blood mononuclear leukocytes, mainly characterized by Th2 predominance.
The aim of this study was to reveal the features of association polymorphisms of interleukin-1 IL-1 and the antagonist of receptor for interleukin-1 IL-1Ra gene polymorphism in Mongoloids and Caucasoid from Khakassia with HP-associated gastroduodenal pathology (chronic gastritis and gastric ulcer). It was revealed that among Khakasses the most widespread genotypes among Khakasses are СС IL-1β and R4R4 IL-1Ra. The association of СС +3953 and R2R3 genotypes with GU risk in Caucasoids was found.
Due to the fact that nowadays mechanisms of syntropy of pathological conditions and nosological units, united within the metabolic syndrome, remain unclear, the scientific review attempts to summarize data on the role of fatty tissue inflammation in pathogenesis of this symptom complex. The results of recent major foreign studies on evaluation of pro-inflammatory activity of adipocytes and macrophages of the fatty tissue, as well as the data on peculiarities of their interactions in abdominal obesity, which is the main component of the metabolic syndrome, were analyzed. Studing pathogenesis of fatty tissue inflammation from the perspective of evaluation of disorders in cell cooperation will allow to more deeply understand cellular and molecular mechanisms of this process as well as open new avenues for developing new pathogenetically justified approaches to metabolic syndrome treatment.
Very little research is devoted to the study of communication systemic immunological changes and local immunological changes in the tissue of the thyroid in autoimmune thyrophaties. The goal of the research was to establish immunologic and morphologic predictors of clinical course and functional outcomes of Graves’s disease (GD).Material and methods. We examined 45 patients with GD (14 men and 31 women) aged 18–55 years (47.0 (35.0–53.0)) years, matching the following criteria: a verified diagnosis GD, accommodation in Tomsk oblast and the Tomsk not less than 10 years, the patient's consent for the study. The control group included 30 people, with an average age of (45.3 ± 5.6) years and was comparable by age and sex with GD patients. The study included: definition of the standard for GD hormonal and serological profile (free T4, free T3, and TSH, antibodies to TPO, antibodies to the TSH receptor), the cultivation of mononuclear leukocytes in complete culture medium within 24 hours with subsequent determination of interleukins concentrations (IL-2, IL-4, TNF-alpha) in culture medium using enzyme-linked immunosorbent assay, determination of the number of blood cells carrying membrane-bound receptors to IL-2, IL-4, TNF-R1 by flow laser cytometry on cytometer BD FACS Canto tmΙΙ (USA) using labeled monoclonal antibody, the standard postoperative histological examination of thyroid gland tissue samples and immunohistochemical detection in samples of thyroid tissue receptors to IL-2, IL-4, TNF-alpha.Results. On the basis of the received results it is possible to allocate 2 clinical-immunologic and morphologic cluster of autoimmune hyperthyroidism syndrome in patients with clinical diagnosis of GD. The first includes the formation of 1 and 2 histological options GD (minimally expressed monocytes infiltration, lack of oncocytic transformation of thyroid epithelium), with some clinical characteristics (persistent and pronounced hyperthyroidism, the large size of goiter, higher titer of receptor TSH-antibody and smaller TPO-antibody, diffuse nature of the lesion), and the second – is represented by 3d histological option with oncocytic restructuring of follicular epithelium, expressed the monocyte/macrophage infiltration with the TNF-RI expression and clinical patterns, including: the older age group of patients, the smaller size of goiter, the emergence of “pseudo nodes” ultrasound, reflecting the presence of lymphoid follicles-infiltrates, more lenient for hyperthyroidism. Probably, that the 2nd cluster is a combination of “classical GD” with autoimmune thyroiditis, however, a set of clinical and laboratory-instrumental signs led to the fact that these patients were in the group of GD patients.Conclusion. This approach (combining study of indicators of systemic and local tissue-specific autoimmune inflammation) is a promising from the point of view of separate parts coverage in the autoimmune thyroids diseases pathogenesis, approximating researchers to develop immune based therapeutic technologies.
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