Резюме. Исследовано влияние трех штаммов пробиотических бактерий: Lactobacillus rhamnosus K32 (L), Bifidobacterium longum GT15 (B), Enterococcus faecium L-3 (E), на уровни экспрессии и содержания ключевых цитокинов при помощи полимеразной цепной реакции с обратной транскрипцией и иммуноферментного анализа соответственно. В работе использованы культура клеток промоноцитарного происхождения (HTP-1) и экспериментальная модель дисбиоза кишечника. В геномах штаммов В и E ранее были выявлены гены, кодирующие бактериоцины, гены компонентов внешней мембраны, пилей и экзополисахаридов, участвующих в модуляции иммунной системы. При исследовании влияния пробиотических штаммов и их супернатантов на экспрессию цитокинов на культуре клеток выявлено увеличение экспрессии TNFα, обусловленное B, E и супернатантом L. Культура В дополнительно вызывала экспрессию IL-8 и IL-10. При коррекции дисбиоза кишечника у крыс (индуцированного метронидазолом и ампициллином) пробиотиками было показано, что нарушение в составе микробиоты (чрезмерный рост Klebsiella spp., низкое содержание Faecalobacterium prausnitzii) оставались у животных после введения L, как в контроле (без введения пробиотиков). В отличие от этих групп у крыс после введения E и B были выявлены: 1) низкие уровни экспрессии провоспалительных цитокинов (IL-8, TNFα, MCP-1) в брыжеечных лимфатических узлах и содержание данных факторов в сыворотке крови; 2) увеличение содержания в сыворотке крови антивоспалительного цитокина TGF-β. В данной работе, при помощи двух взаимодополняющих моделей, выявлены индивидуальные особенности иммуномодулирующих эффектов пробиотических штаммов L. rhamnosus K32, B. longum GT15 (B), E. faecium L-3, оказывающих различное влияние на микробиоту кишечника.
Our objective was to develop a model of systemic inflammatory response syndrome (SIRS) by chemical induction of colon injury and antibiotic-associated intestinal dysbiosis in rats with primary visceral obesity (PVO) for studies of myocardial resistance to ischemia-reperfusion injury. The experiments were performed with adult Wistar male rats with PVO under improved conditions of a conventional animal clinic. The chemically induced inflammatory colon disease (CIICD) was accomplished by intragastric administration of a mixture of broad-spectrum antimicrobial agents (AMA) for 3 days. Five days later, immunological and biochemical studies were carried out, as follows: composition of the intestinal microbiota in feces and shortchain fatty acids in blood, morphological changes in the structure of the colon, hemodynamic parameters and myocardial stability with modified Langendorff system. In PVO rats, the mass of visceral fat deposits and the content of lipopolysaccharides (LPS) in the blood were significantly increased when giving them fatcarbohydrate diet (FCD). In animals with CIICD, in addition to LPS, there was a significant increase in proinflammatory cytokine concentration (TNF, IL-8, MCP-1), and after oral administration of the AMA mixture, pronounced disturbances of food behavior and evacuatory function of gastrointestinal tract, deep destructive changes in colon, as well as qualitative and quantitative composition of intestinal microbiota with characteristics typical to the first-grade dysbiosis. High levels were shown for IL-8 cytokine only. An increase in acetic and propionic acid concentrations were shown in blood in animals with CIICD, and, to a greater extent, in rats with antibiotic-induced dysbiosis (AID). FCD was followed by significantly reduced levels of lactobacilli and bifidobacteria in colonic contents. CIICD leads to detection of Escherichia coli, and intestinal dysbiosis leads to the manifestation of Proteus. A comorbid combination of pathological changes in the immune and digestive systems caused a significant increase in the area of myocardial necrosis (by 35 percent) in isolated heart by, thus presuming decreased myocardial resistance to ischemia-reperfusion injury (IRI). The SIRS model induced by chemical trauma to large intestine is aggravated by the introduction of AMAs mixture, and it is characterized by a controlled change in inflammatory markers. Deterioration of morphofunctional characteristics in isolated heart included decrease in resistance to IRI seems to correspond to acute inflammatory bowel disease with induced intestinal dysbiosis. This model can be used in experimental medicine in the field of cardiology, endomicroecology, gastroenterology, and immunology.
This article presents a view of heart transplantation from asystolic donors. Based on the recent evidence of modern research, the difficulties in heart transplantation from donors of this category are described. This article presents a classification of asystolic donors, specifies the features of each category in relation to heart donation. Based on the recent evidence of modern knowledge about asystolic donors, possible methods of assessment and management protocols for donors are presented. The article may be of interest to pathophysiologists, transplantologists, cardiologists, and medical students.
Background: Myocardial infarction (MI) is one of the leading causes of mortality in patients with type 2 diabetes mellitus (DM), therefore it is essential to give preference to a glucose-lowering drug having optimal cardioprotective properties. A comparative study of the various sodium-glucose co-transporter inhibitors representatives’ protective effects in experimental MI was not carried out within the framework of one study.Aim: To evaluate the influence of empagliflozin (EMPA) and canagliflozin (CANA), in comparison with sitagliptin (SITA), on hemodynamic parameters and myocardial damage area in rats with diabetes type 2 model in experimental MI.Materials and methods: Type 2 DM was modelled in Wistar rats by means of 4-week high-fat diet followed by nicotinamide 230 mg/kg and streptozotocin 60 mg/kg administration. 4 weeks after DM induction the following groups were made: «DM+SITA» — treatment with SITA 50 mg/kg, «DM+EMPA» — treatment with EMPA 2 mg/kg, «DM+CANA» — treatment with CANA 25 mg/kg per os once daily for 8 weeks. Animals in «DM» group remained untreated for the following 8 weeks. Rats in control group were fed with standard chow. 16 weeks after the experiment beginning transient global myocardial ischemia was modelled in all rats. Hemodynamic parameters and myocardium necrosis area were evaluated.Results: The necrosis area was larger in «DM» group, than in control one (p=0.018). Infarction size in «DM+SITA» did not differ from that in «DM» group (62.92(41.29;75.84) and 57.26(45.51;70.08)%, р=0.554). Necrosis area in «DM+EMPA» and «DM+CANA» groups was smaller than in «DM» group (37.90(20.76;54.66)%, 46.15(29.77;50.55) vs 57.26(45.51;70.08)%, р=0.008 and р=0.009, respectively). Necrosis size did not differ between «DM+EMPA» and «DM+CANA» groups (p=0.630). Ischemic contracture in «DM+CANA» group was less prominent than under the use of all other glucose-lowering drugs. We observed increase of coronary blood flow in «DM+EMPA» group, in comparison with «DM», «DM+CANA» and «DM+SITA» groups.Conclusions: SITA does not have cardioprotective effect in ischemia-reperfusion injury in diabetic rats. EMPA and CANA have similarly prominent infarct-limiting properties. EMPA is able to increase coronary blood flow, whereas cardioprotective action of CANA is associated with ischemic contracture diminishing.
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