Sirtuins, class III histone deacetylases, are involved in the regulation of tissue repair processes and brain functions after a stroke. The ability of some isoforms of sirtuins to circulate between the nucleus and cytoplasm may have various pathophysiological effects on the cells. In present work, we focused on the role of non-mitochondrial sirtuins SIRT1, SIRT2, and SIRT6 in the restoration of brain cells following ischemic stroke. Here, using a photothrombotic stroke (PTS) model in mice, we studied whether local stroke affects the level and intracellular localization of SIRT1, SIRT2, and SIRT6 in neurons and astrocytes of the intact cerebral cortex adjacent to the ischemic ipsilateral hemisphere and in the analogous region of the contralateral hemisphere at different time points during the recovery period after a stroke. We evaluated the co-localization of sirtuins with growth-associated protein-43 (GAP-43), the presynaptic marker synaptophysin (SYN) and acetylated α-tubulin (Ac-α-Tub), that are associated with brain plasticity and are known to be involved in brain repair after a stroke. The results show that during the recovery period, an increase in SIRT1 and SIRT2 levels occurred. The increase of SIRT1 level was associated with an increase in synaptic plasticity proteins, whereas the increase of SIRT2 level was associated with an acetylated of α-tubulin, that can reduce the mobility of neurites. SIRT6 co-localized with GAP-43, but not with SYN. Moreover, we showed that SIRT1, SIRT2, and SIRT6 are not involved in the PTS-induced apoptosis of penumbra cells. Taken together, our results suggest that sirtuins functions differ depending on cell type, intracellular localization, specificity of sirtuins isoforms to different substrates and nature of post-translational modifications of enzymes.

The article presents the results of a clinical and bacteriological assessment of the pharmacological efficacy of 1,3-diethylbenzimidazolium triiodide in chronic compensated tonsillopharyngitis. As a result of a 10-day course of treatment, an improvement in the clinical status of patients was achieved, as well as a significant positive effect on the composition of the pharyngeal microbiocenosis. In particular, the content of Staphylococcus aureus, β-hemolytic streptococci, Escherichia signifi cantly decreased, and Enterobacteria, non-fermenting bacteria, and Streptococci pneumonia completely disappeared from the microbial focus. However, the conducted 10-day treatment did not lead to the complete disappearance of α-hemolytic and non-hemolytic streptococci from the microbial population. This may be explained by the reparative effect of Stellanin® on the lymphoid formations of the pharynx, contributing to the restoration of colonization resistance.

This review analyzed the literature data on the in vitro preclinical study of the cytotoxic properties of organotin compounds, as well as the main mechanisms of their action. The latter consist in interacting with SH groups of proteins, initiating oxidative stress, binding to DNA, interacting with receptors, as well as activate apoptosis by increasing the expression of caspases, proapoptotic proteins, and decreasing antiapoptotic proteins. Organotin compounds, depending on the donor ligand, exhibit specifi c cytotoxicity towards certain tumor cell lines. The high cytotoxic potential indicates the possibility of further development in vivo and research of organotin compounds as candidates for the creation of drugs for anticancer and antimetastatic therapy.

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