No abstract

Novel silver/poly-1-vinyl-1,2,4-triazole nanocomposite materials—possessing antimicrobial activity against Gram-positive and Gram-negative bacteria—have been synthesized and characterized in the solid state and aqueous solution by complex of modern physical-chemical and biologic methods. TEM-monitoring has revealed the main stages of microbial cell (E. coli) destruction by novel nanocomposite. The concept of direct polarized destruction of microbes by nanosilver proposed by the authors allows the relationship between physicochemical and antimicrobial properties of novel nanocomposites. At the same time, it was shown that the nanocomposite was nontoxic to the fibroblast cell culture. Thus, the synthesized nanocomposite combining antibacterial activity against Gram-positive and Gram-negative bacteria as well as the absence of toxic effects on mammalian cells is a promising material for the development of catheters, coatings for medical devices.

No abstract

We studied the effect of VEGF-A in experimental myocardial infarction on attraction of progenitor cells into the regeneration zone. The appearance of CD34(+)CD45(+) cells known as low-differentiated progenitor cells was observed in the damaged myocardial tissue in the presence of a considerable excess of VEGF-A. These cells can act as precursors of mesenchymal tissues depending on the direction of differentiation.

В настоящее время распространенность па-тологий, при которых избыточный рост соеди-нительной ткани является одним из основных факторов патогенеза (кардиосклероз и связанная с ним сердечная недостаточность, контрактуры суставов, спаечная болезнь, пневмосклероз, цир-УДК 611-018.2:577.112 DOI: 10.20538/1682DOI: 10.20538/ -0363-2017 Для цитирования: Шурыгина И.А., Шурыгин М.Г., Зеленин Н.В., Аюшинова Н.И. Воздействие на митогенактивируемые протеинкиназы как новое направление регуляции роста соединительной ткани. Бюллетень сибирской медицины. 2017; 16 (4): 86-93.Воздействие на митогенактивируемые протеинкиназы как новое направление регуляции роста соединительной ткани Шурыгина И.А., Шурыгин М.Г., Зеленин В.Н., Аюшинова Н.И. Россия, 664003, г. Иркутск, ул. Борцов Революции, 1 РЕЗЮМЕ В обзоре представлена современная классификация, функции основных групп митогенактивируемых протеинкиназ (МАРК). Приведены данные о путях их активации и функционирования. Основное вни-мание уделено семейству р38 МАРК. В обзоре воздействие на данные сигнальные каскады рассмотрено как перспективное направление воздействия на рост соединительной ткани. В этом аспекте обобщен мировой опыт по активации и блокаде внутриклеточных каскадов. Обобщен собственный опыт работы в данном направлении. В частности продемонстрировано, что стимуляция р38 МАРК при подавлении активности JNK каскада ведет к ускоренному образованию соединительной ткани в зоне послеопера-ционного хирургического рубца, доказана возможность управления ростом соединительной ткани при воздействии на МАР-киназные каскады. Пролонгированная блокада р38 МАРК снижает ширину кожно-го рубца и плотность коллагеновых волокон в зоне формирования послеоперационного рубца, снижает интенсивность спайкообразования в брюшной полости при травме брюшины. Иркутский научный центр хирургии и травматологии (ИНЦХТ)Таким образом, учитывая важную роль и универсальность МАР-киназных механизмов регуляции кле-точного роста и дифференцировки, перспективно изучение участия данных механизмов в универсаль-ных биологических процессах, таких как воспаление, апоптоз, регенерация, а также разработка на этой основе способов управления течением этих процессов. Использование стимуляторов и блокаторов МАР-киназных механизмов перспективно как новое направление в лечении многих заболеваний, патоге-нез которых связан с нарушением клеточной дифференцировки, пролиферации, избыточной выработки цитокинов, управлением ростом соединительной ткани.Ключевые слова: митогенактивируемая протеинкиназа, р38 МАРК, JNK MAPK, ERK МАРК, инги-битор МАРК, соединительная ткань.

The relationship between vascular endothelium growth factor (VEGF) and cardiomyocyte oxidative phosphorylation level in experimental myocardial infarction, caused by diathermocoagulation of the periconical ventricular artery, was studied by immunofluorescent microscopy. Staining showed uneven distribution of cytochrome c in the mitochondria in the focus of myocardial infarction 2 h after the operation. After 24 h uneven staining of cardiomyocytes was found in the peri-infarction zone and no staining in the zone of myocardial infarction. This indicated a significant decrease in the level of redox enzymes. This picture persisted till day 14. Intraventricular injection of VEGF to animals led to a significant increase of the immunohistochemical reaction intensity, which reached the peak by day 7. The distribution of immunohistochemical reaction products under conditions of VEGF blocking was about the same as in spontaneous postinfarction reparative restitution. Our data indicated that increase of VEGF concentration in the myocardium maintained and stimulated oxidative phosphorylation in cardiomyocytes during the postinfarction period.

Background: Apoptosis, one of the most important mechanisms for maintaining homeostasis, is carried out under both physiological and pathological conditions. The aim of our study was to investigate the expression of markers of apoptosis through caspase-dependent and caspase-independent pathways during the reparative regeneration after serosal injuries of the peritoneum in the context of the prolonged p38 MAPK inhibition. Methods: Peritoneal adhesions in the animal models were induced by a method developed by the authors that included opening the serous-muscular layer of the caecum with a 1cm cut followed by closing the wound with a Schmieden suture and scarifying a 1.5×1.5 cm area of the parietal peritoneum of the right lateral channel. Experiments were carried out on male 9-monthold Wistar rats. When closing the wound, control animals were intraperitoneally administered 3 mL of 0.9% sodium chloride solution (n=40) while experimental group rats were administered slow-release drug Seroguard ® (Pharmasyntez JSC) (n=40). Animals were sacrificed within the period of 2 hours to 30 days post surgery. Expression of apoptosis markers was studied by immunohistochemical (Bcl-2, Bcl-xl) and immunofluorescent (PARP-1) staining. Results: It is interesting that, in cases of the natural regeneration of the peritoneal injury, expression of anti-apoptosis markers at the injury site came in two waves: it was the most pronounced on days 1-3 post surgery while the second peak of activity was observed on day 14. Within this time window, granulation tissue was actively growing and mature connective-tissue vascularized adhesions were being formed. By the end of the observation period (day 30), expression of anti-apoptosis proteins at the injury site became extremely low and a significant reduction in the amount of connective tissue cells was observed. It was found that a prolonged inhibition of the p38 activity resulted in a moderate increase in Bcl-2 expression on days 3-7, and a decrease in the activity on day 14 was followed by another increase in expression by day 30. The Bcl-xl expression was observed 12 hours to 3 days post surgery and then it went down to the minimum. Positive PARP-1 staining observed on days 3 to 30, which reached its maximum on day 14, was also typical of the experimental group. Conclusion: The performed study demonstrated that a prolonged p38 MAPK inhibition in the adhesion formation models results in the activation of fibroblast apoptosis at the reparation site, which, in the authors' opinion, predetermines a significant decrease in the adhesion formation in the experimental group.

No abstract