ГЕНДЕРНЫЕ ОСОБЕННОСТИ ВЗАИМОСВЯЗИ ГОРМОНАЛЬНОЙ АКТИВНОСТИ ЖИРОВОЙ ТКАНИ И ПРОВОСПАЛИТЕЛЬНОГО СТАТУСА ПРИ ГИПЕРТОНИЧЕСКОЙ БОЛЕЗНИ С МЕТАБОЛИЧЕСКИМ СИНДРОМОМ

Objective: research gender features of relationship of hormonal activity of adipose tissue and proinflammatory status with essential hypertension (EH) in combination with metabolic syndrome (MS).Material and methods. Were examined 46 patients with essential hypertension stage (BP < 180/110 mm Hg.) in conjunction with the metabolic syndrome. Along with a complete clinical, laboratory and instrumental examination adopted in specialized cardiological clinic, were defined concentrations in serum leptin, adiponectin, resistin and visfatin and the level of markers of systemic inflammation (C-reactive protein, neopterin and fibrinogen), was assessed the level of spontaneous production of cytokines and active oxygen species and the expression level of CD4, CD8 and CD36 – blood mononuclear leukocytes markers.Results and conclusions. It was established that the hormonal status of adipose tissue have women with EH combined with MS are characterized by higher levels of leptin and adiponectin in blood serum than in men.It was established not only a significant role adipokin imbalance in mechanisms of MS and systemic inflammation in these patients category, but also were studied gender characteristics. While for men in the development of the above pathological manifestations hipoadiponektinemia has the most meaning, and for women – hyperleptinemia.Цель исследования – изучить особенности взаимосвязи гормональной активности жировой ткани и провоспалительного статуса при гипертонической болезни в сочетании с метаболическим синдромом у мужчин и женщин.Материал и методы. Обследовано 46 пациентов с гипертонической болезнью (ГБ) (артериальное давление менее 180/110 мм рт. ст.) в сочетании с метаболическим синдромом (МС). Наряду с полным клиническим, лабораторным и инструментальным обследованием, принятым в специализированной кардиологической клинике, определялись концентрации в сыворотке крови лептина, адипонектина, резистина и висфатина и уровень маркеров системного воспаления (С-реактивного белка, неоптерина и фибриногена), оценивался уровень спонтанной продукции цитокинов (IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, TNFα, INFγ и МСР-1) и активных форм кислорода, а также уровень экспрессии CD4-, CD8- и CD36-маркеров мононуклеарными лейкоцитами крови.Результаты. Установлено, что гормональный статус жировой ткани у женщин с ГБ в сочетании с МС характеризуется более высоким уровнем лептина и адипонектина в сыворотке крови, чем у мужчин.Определены значительная роль адипокинового дисбаланса в механизмах МС и системного воспаления у данной категории больных и гендерные особенности. При этом для мужчин в развитии вышеперечисленных патологических проявлений наибольшее значение имеет гипоадипонектинемия, а для женщин – гиперлептинемия.

НАРУШЕНИЯ МЕЖКЛЕТОЧНЫХ ВЗАИМОДЕЙСТВИЙ В ПАТОГЕНЕЗЕ ВОСПАЛЕНИЯ ЖИРОВОЙ ТКАНИ ПРИ МЕТАБОЛИЧЕСКОМ СИНДРОМЕ

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.Ввиду того что в настоящее время остаются недостаточно ясными механизмы синтропии патологических состояний и нозологических единиц, объединенных рамками метаболического синдрома, в научном обзоре предпринята попытка обобщить данные о роли воспаления жировой ткани в патогенезе этого симптомокомплекса. Проанализированы результаты крупных зарубежных исследований последних лет, посвященных оценке провоспалительной активности адипоцитов и макрофагов жировой ткани, а также данные, касающиеся особенностей их взаимодействия при абдоминальном ожирении – основном компоненте метаболического синдрома. Изучение патогенеза воспаления жировой ткани с позиций оценки нарушений кооперации клеток позволит глубже понять клеточные и молекулярные механизмы этого процесса и открывает перспективы для разработки новых патогенетически обоснованных подходов к лечению метаболического синдром

Efficacy of Synthetic Peptide Corresponding to the ACTH-Like Sequence of Human Immunoglobulin G1 in Experimental Autoimmune Encephalomyelitis

Peptide immunocortin sequence corresponds to the amino acid residues 11–20 of the variable part of human immunoglobulin G1 (IgG1) heavy chain. Since immunocortin was shown previously to inhibit phagocytosis in peritoneal macrophages and ConA-induced T-lymphocytes proliferation in culture, we suggested that immunocortin administering may be of use for patients with self-immune syndrome. Immunocortin in concentration 10 μM inhibited proliferation of both antigen (myelin)-induced and ConA-induced LN lymphocytes isolated from the lymph nodes of Dark Agouti (DA) rats immunized with chorda shear. The biological trials of the synthetic immunocortin were carried out on the DA rats with induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. These in vivo experiments have shown that intraperitoneal injections of immunocortin in a daily dosage 100 μg per animal reduced symptoms of EAE in DA rats

SUBPOPULATIONS AND METABOLIC ACTIVITY OF BLOOD MONONUCLEAR CELLS IN METABOLIC SYNDROME

Aim of study: to examine the features of expression of CD-markers of blood mononuclear leukocytes and their functional activity in the metabolic syndrome. Conducted a cross-sectional (transverse) study of 76 patients with essential hypertension (EH) II stage (BP <180/110 mm Hg.) [10] in conjunction with the metabolic syndrome and 20 people, formed the control group. Along with a complete clinical, laboratory and instrumental examination taken in a specialized cardiological clinic was conducted determination of surface markers of lymphocytes CD4+, CD8+ and monocytes CD36+ and assessment of the level of spontaneous production of reactive oxygen blood mononuclear leukocytes. Found that in patients with the metabolic syndrome compared with the control group the proportion of CD4+ lymphocytes and the level of spontaneous ROS production by mononuclear leukocytes significantly higher. The positive correlated interconnection between these indicators and the number of CD36+ monocytes with the majority of clinical and metabolic markers of MS confirmes their participation in mechanism of immune inflammation and oxidative stress in this pathological process

EFFECTS OF AN EIGHT-WEEK ATORVASTATIN TREATMENT ON SPONTANEOUS CYTOKINE PRODUCTION BY THE BLOOD MONONUCLEAR LEUKOCYTES IN METABOLIC SYNDROME

The aim of this study was to assess effects of the eight-week course of atorvastatin therapy upon the levels of spontaneous cytokine production by mononuclear blood leukocytes (MNBC) in metabolic syndrome. An open-label prospective study included 36 patients with stage II hypertension (blood pressure < 180/110 mm Hg.) accomplished by metabolic syndrome. Along with clinical surveys performed at a specialized cardiological clinics, we assessed spontaneous cytokine production by MNBC during treatment with atorvastatin. It was shown that the 8-week treatment of these patients with atorvaststin, at individually matched daily doses (20to 40 mg) was associated with reduced serum concentration of acute phase proteins (C-reactive protein and neopterin), as well as decreased spontaneous production of proinflammatory cytokines (IL-1β, IL-6 and TNFα) by MNBCs. The latter finding is of great importance for pathogenesis of metabolic syndrome

DISORDER OF INTERCELLULAR CORRELATIONS IN PATHOGENESIS OF FATTY TISSUE INFLAMMATION IN METABOLIC SYNDROME

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