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To identify the effect of probiotic (PB) on cytokines profile in knee cartilage of rats with experimental osteoarthritis (OA). Methods. The animals of 1 st (Сontrol) and 3 rd (PB) groups got 50 µL of saline to both hind knees. The animals of 2 nd (MIA-OA) and 4 th groups (MIA-OA-PB) got single injection of 1 mg monoiodoacetate (MIA) dissolved in 50 µL of saline to knee, after which MIA-OA developed for 28 days. PB feeding [was] provided daily for 14 days during the MIA-OA progress. The levels of cytokines (IL-1β, TNF-α, IL-6, IL-8, IFN-γ, IL-4, IL-10, TGF-β, IGF-1) were measured in cartilage homogenates by [the] enzyme-linked immunosorbent assay (Biotrak ELISA System, GE Healthcare, USA). Results. MIA-OA caused [an] increase in the levels of IL-1β, TNF-α, IL-6, IL-8, IFN-γ, IL-10, TGF-β, decreased the level of IGF-1 and did not change the level of IL-4, compared to Control. PB during MIA-OA increased the level of IGF-1, decreased the levels of IL-1β, TNF-α, IL-6, IL-8, IFN-γ, TGF-β, compared to MIA-OA, but did not reach the Control values (unlike IL-4 and IL-10 that equaled to Control). Conclusions. MIA-OA caused significant changes in the levels of studied cytokines in knee cartilage. An application of PB has positive local anti-inflammatory effect in cartilage tissue of rats with MIA-OA.

Background. Scorpion stings may be life-threatening since their venoms are comprised of a wide range of toxins and other bioactive molecules, such as enzymes. At the same time, scorpion envenomation may increase matrix metalloproteases (MMPs) levels, which enhance proteolytic tissue destruction by venom. However, investigations on the impact of many scorpions’ venoms, such as those of Leiurus macroctenus, on tissue proteolytic activity and MMP levels have not yet been conducted. Methods and Results. The present study aimed to examine the total proteolysis levels in various organs after Leiurus macroctenus envenomation and evaluate the metalloproteases and serine proteases’ contributions to the total proteolytic activity. Changes in MMPs and TIMP-1 levels were tested as well. Envenomation led to a significant increase in proteolytic activity levels in all assessed organs, mostly in the heart (by 3.34 times) and lungs (by 2.25 times). Conclusions. Since EDTA presence showed a noticeable decrease in total proteolytic activity level, metalloproteases appeared to play a prominent role in total proteolytic activity. At the same time, MMPs and TIMP-1 levels were increased in all assessed organs, suggesting that Leiurus macroctenus envenomation causes systemic envenomation, which may induce multiple organ abnormalities, mostly because of the uncontrolled metalloprotease activity.

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The accumulated data indicate that a high level of homocysteine may be a central pathogenetic factor of chronic obstructive pulmonary disease. In this study, we investigated the effect of hyperhomocysteinemia on protein homeostasis in the rat lungs. The level of proteins, peptides, total proteolytic activity, as well as protein-peptide composition, were evaluated. Hyperhomocysteinemia was induced by daily intragastric administration of DL-homocysteine thiolactone (100 mg·kg-1 of body weight) to albino non-linear male rats for 28 days. Twelve hours after the last administration, the rats were sacrificed and the lungs were harvested. Our findings showed that hyperhomocysteinemia caused the disturbances in the protein homeostasis in the lungs that are manifested by a decrease in the level of proteins in the young and old animals and an increase in the level of peptides in the rats of all studied groups. We found a change in the protein composition in the lung of HM rats - a decrease in the level of proteins with a molecular weight of 50 kDa to 100 kDa simultaneously with an increase in the level of proteins with a molecular weight of less than 50 kDa. Despite the fact that the peptide profile was the same in both control animals and HM animals, the level of individual peptide fractions increased significantly in the rats with HM. Obtained data could contribute to explain, at least in part, the mechanisms involved in the pathogenesis of lung damage in hyperhomocysteinemia.