Search

Background: Osteoarthritis (OA) is a common worldwide disease induced by a wide range of biochemical processes, mainly inflammation and degradation of collagen. The aim of this study, was to describe the effect of a multistrain probiotic (PB) and chondroitin sulfate (CS), administered separately or in combination, on the expression of Ptgs2, Tgfb1 and Col2a1 during monoiodoacetate-induced OA in male rats., Methods: OA was induced in male rats by injecting monoiodoacetate in right hind knee. Therapeutic groups received 3 mg/kg of CS for 28 days and/or 1.4 g/kg of multistrain PB for 14 days. Knee cartilage were taken 30 days after monoiodoacetate injection. RNA was extracted and the expression of Ptgs2, Tgfb1 and Col2a1 were analyzed using SYBR Green 1-step real-time quantitative polymerase chain reaction., Results: Induction of OA caused an upregulation in Ptgs2, Tgfb1 expression, and downregulation of Col2a1. Separate administration of PB and CS reduced Ptgs2 and Tgfb1 expressions. Their combined administration significantly decreased the expression of these pro-inflammatory cytokines, comparable to controls. Expression of Col2a1 showed similar behavior, with upregulation in therapeutic group with separate administration and the cumulative effects in case of co-administration., Conclusions: The multistrain PB diet may offer a perspective to improve the standard treatment of OA and, necessitates further investigation with clinical trials.

Expression of Tlr2, Muc2, Defa genes in rat duodenal upon long-term gastric hypacidity (hypochlorhydria) and with multiprobiotic correction was investigated. Increasing of Tlr2, Muc2, Defa expression on the background of the intensification of lipid peroxidation in rat duodenal villus and crypt epithelial cells upon gastric hypoacidity was shown. The mRNAs patterns of genes mentioned above were shown to decrease or approach to control values as well as the level of lipid peroxidation products under the treatment of hypoacidic rats with the multiprobiotic. The data obtained may indicate involvement of genes Tlr2, Muc2, Defa in development of inflammation in the duodenum due to dysbiotic changes under conditions of prolonged hypochlorhydria.

We investigated the preventive effect of low molecular weight organic compound 2-(2-hydroxyphenoxy) acetyl-L-prolinat sodium on erosive and ulcerative lesions in the gastric mucosa caused by stress. It was established that prophylactic administration of this substance to rats at a dose of 1 mg/kg reduced the lesion area by 56.7%. 2-(2-hydroxyphenoxy) acetyl-L-prolinat sodium efficiently restored the impaired pro-/antioxidative balance in the gastric mucosa of rats under stress: the content of diene conjugates was reduced by 1.24 times, TBA-active products reduced by 1.31 times, Schiff's bases reduced by 1.28 times. This effect was accompanied by increased activities of the superoxide dismutase, catalase and of glutathione system.

Free-radical processes upon long-term omeprazole-induced gastric hypochlorhydria in the rat liver were researched. Intensification of oxidative processes in the liver tissue upon gastric hypoacid state was established: overproduction of superoxide anion, hydrogen peroxide, the quantitative changes of lipid functional groups, increased level of lipid peroxidation products, and augmentation of xanthine oxidase activity. The expression of Tgfb1 gene increased, while the expression of Hgf gene was not detected upon long-term suppression of gastric acid secretion of hydrochloric acid by omeprazole that indicated possible development of liver fibrosis. Abovementioned parameters were only partially restored to control values in the case of simultaneous administration of multiprobiotic "Symbiter acidophilic" concentrated with omeprazole, thus indicating the ability of this preparation to counteract the development of oxidative damages in liver tissues upon long-term gastric hypoacidic conditions.

The intensity of free-radical processes upon long-term omeprazole-induced hypoacidity in the rat pancreas was investigated. Significant violation of oxidative-antioxidative balance in pancreatic tissue upon gastric hypochlorhydria was established: overproduction of superoxide anion, quantitative changes of lipid functional groups, increased level of lipid peroxidation products, augmentation of xanthine oxidase, superoxide dismutase and glutathione transferase activity, as well as depletion of catalase, glutathione peroxidase activity and reduced glutathione content. The inflected expression of Cckbr gene in the rat pancreas upon these conditions was also observed, thus suggesting an increased risk of pathological changes development in the gland. Abovementioned parameters were only partially restored to control values in the case of simultaneous administration of multiprobiotic "Symbiter" with omeprazole, thus indicating the ability of this preparation to efficiently counteract the development of oxidative damages in pancreatic tissues upon long-term hypoacidic conditions.

The lipid peroxidation state and the system functioning of antioxidant protection in parietal cells under rat chronic atrophic gastritis development was investigated. It was detected that the compensatory increase of superoxide dismutase and catalase activity did not affect the lipoperoxidation process and this resulted in accumulation of toxic TBA reactive substances and diene conjugates during the whole stages of the experimental pathology development. It was shown that the reserved power of the glutathione antioxidant system is sufficient to provide adoptable response in the acute period of the disease owing to increasing intracellular found of the reduced glutathione, but it is insufficient to prevent its decreasing in parietal cells in case of the chronic atrophic gastritis development. Our findings suggest that glutathione system is involved in processes of gastric atrophy. The obtained results testify about considerable system dysfunctions of lipid peroxidation and the antioxidant protection in processes of the rat experimental atrophic gastritis development.