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Burn injuries are a type of traumatic pathology that is characterized by a complex set of polysystemic shifts. The body's response to a burn injury corresponds to the mechanism of the stress response with the development of the adaptation syndrome, resulting in disruption of the normal flow of oxidizing processes [6]. Oxidizing modification of proteins (OMP) is one of the early and most reliable indicators of tissue damage in case of a free radical pathology. These are proteins but not lipids or nucleic acids that are effective traps of the generated reactive oxygen species (ROS) and their oxidizing modification is regarded as one of early and reliable markers of the oxidizing stress [1, 9]. The oxidates of proteins in oxidizing damages in tissues appear earlier and are more stable compared to the products of lipid peroxidation, in particular plasma proteins subjected to oxidizing degradation having quite long half-life. [1] OMP causes changes in physical and chemical properties of the protein molecule: the fragmentation, aggregation and susceptibility to pro-te olysis [2, 8]. As a result, either the formation of products with a high functional activity or either inactivation of zymophores, or modification of protein molecules, that can have a toxic effect and aggravate the pathologic process, occur. The pres ence of ROS in the wound de fect leads to dena tu ra tion of the syn the sized pro tein and in ac ti va tion of fi bro blasts that im pede wound heal ing [9]. The study of the bio chemi cal as pects of the de vel op ment of a burn injury is nec es sary to gen er ally un der stand the mecha nisms of the heal ing pro cess and de velop a strat egy for its treatment and de vel op ment of new wound heal ing medi cines that af fect the ma jor ity of patho logic links of the wound pro cess. In most stud ies, de voted to the mecha nisms of de vel op ment of a burn wound, the con tent of lipid per oxida tion prod ucts is ana lyzed, the con cen tra tion of oxi dized pro teins is vir tu ally paid no at ten tion [6,7]. The aim of this study is to examine the state of oxidizing modification of proteins in the treatment with new wound healing preparations at the model of the third A-degree burn injury in rats. MATERIALS AND METHODS A model of a burn injury was reproduced on 168 mature male albino rats weighing 200-240 g. In animals, under general anesthesia using thiopental (40 mg/kg) on the depilated skin area on the back, retreating from the spine for 1.5 cm, a burn was simulated with an instrument

Aim: To evaluate the effects of orally administered gadolinium orthovanadate GdVO4:Eu3+ nanoparticles (VNPs) on the course of chronic carrageenan-induced intestinal inflammation. Methods: Samples of small intestinal tissue were collected from four groups of rats (intact, after administration of VNPs, with carrageenaninduced intestinal inflammation, with carrageenan-induced intestinal inflammation orally exposed to VNPs) to assess the intestinal morphology and HSP90α expression. Levels of seromucoid, C-reactive protein, TNF-α, IL-1β and IL-10 were determined in blood serum. Results: Oral exposure to VNPs was associated with neither elevation of inflammation markers in blood serum nor HSP90α overexpression in the small intestine, i.e. no toxic effects of VNPs were observed. Carrageenan-induced intestinal inflammation was accompanied by higher levels of TNF-α and IL-1β, as well as HSP90α upregulation in the intestinal mucosa, compared with controls. Administration of VNPs to rats with enteritis did not lead to statistically significant changes in concentrations of circulating pro-inflammatory cytokines with the trend towards their increase. Conclusion: No adverse effects were observed in rats orally exposed to VNPs at a dose of 20 μg/kg during two weeks. Using the experimental model of carrageenan-induced enteritis, it was demonstrated that VNPs at the dose used in our study did not affect the course of intestinal inflammation.

It was determined that the studied 5-[(Z)-(4-nitrobenzylidene)]-2-(thiazol-2-ylimino)-4-thiazolidinone (Les-6222) affects the cyclooxygenase pathway of the arachidonic acid cascade, the markers of damage to neurons on models of PTZ kindling. In the model of chronic epileptogenesis in mice (pentylenetetrazole kindling), a 4-thiazolidinone derivative showed high anticonvulsant activity, which is weaker than the effect of sodium valproate and higher than Celecoxib. The mentioned compound has a pronounced anti-inflammatory effect in the brain on the background of the PTZ kindling, reliably inhibiting COX-1 and COX-2. The predominant inhibition of COX-2 by 44.5% indicates this enzyme’s high selectivity of Les-6222. According to the molecular docking study results, the studied compound revealed the properties of COX-1/COX-2 inhibitor and especially 5-LOX/FLAP. The decreasing content of 8-isoprostane in the brain of mice of the Les-6222 group indicates a beneficial effect on cell membranes in the background of oxidative stress during the long-term administration of PTZ. In addition, Les-6222 significantly decreased the content of neuron-specific enolase, indicating neuroprotective properties in the background of chronic epileptogenesis. The obtained results experimentally substantiate the feasibility of further developing Les-6222 as a promising anticonvulsant agent.