[Mechanisms of realization of protective effect of miliacin during experimental Salmonella infection: effect of endotoxinemia and cytokine production].

AIM: Evaluate the effect of miliacin on the intensity of endotoxinemia and features of cytokine production in experimental salmonella infection. MATERIALS AND METHODS: The studies were carried out in 128 male mice (CBAxC57Bl6)F1 divided into 4 groups: I--intact; II--infected; III--infected after administration of miliacin solvent: tween-21; IV--infected after administration of miliacin. Determination of the endotoxin in blood plasma was carried out by using chromogenic LAL-test. Cytokine production was studied in splenocyte culture by EIA method. RESULTS: Miliacin reduced the intensity of endotoxinemia in mice of group IV. Salmonella infection increased spontaneous (IFNγ) and induced (IL-12, IFNγ, IL-17) cytokine production. Miliacin ensured the most significant increase of spontaneous IL-10, IL-12 and IFNγ production compared with groups II and III. At the same time it limited the increase of induced IL-17 production compared with groups II and III. CONCLUSION: Protective effect of miliacin is determined by the reduction of endotoxinemia, mobilization of Th-1 response, stimulation of IL-10 production and limitation of IL-17 participation in the development of the inflammatory reaction.

[The natural triterpenoid miliacin prevents methotrexate-induced oxidative stress and normalizes the expression of genes encoding the cytochrome P-450 2E1 isoform and glutathione reductase in the liver].

We studied the role of the natural triterpenoid miliacin (3-3-methoxy-Al8-oleanene) in the regulation of oxidative stress in the liver of (CBAxC57B1(6))F1 mice exposed to methotrexate. Miliacin attenuated methotrexate-induced lipid peroxidation as determined by an attenuation of thiobarbituric acid-reacting products in the liver. Furthermore, miliacin normalized the expression of genes encoding the 2e1 isoform of cytochrome P-450 and glutathione reductase that were dramatically dysregulated by methotrexate. These results established the role of miliacin in modulation of redox genes, thereby providing evidence for a new mechanism of organ protection by this triterpenoid.

[Protective effect of miliacin during experimental salmonellosis infection].

AIM: Evaluation of influence of triterpenoid miliacin on the development of experimental salmonellosis infection. MATERIALS AND METHODS: Studies were carried out in 330 male mice (CBAxC57Bl6)F1. Miliacin was administered 3 times intraperitoneally with the interval of 3 days between administrations at a single dose of 2 mg/kg. The animals were infected intraperitoneally by hospital origin Salmonella enteritidis strain (2x10(6) bacteria per mice). 4 groups of mice were used: I - intact; II - infected; III - infected after administering solvent for miliacin 3 times (tween 21 at final concentration of 1.6x 10(-7) mol/kg); IV - infected after administration ofmiliacin. RESULTS: Miliacin reduced the mortality of mice compared with groups II and III. Microbial contamination of mice spleen in group IV was significantly lower compared with group II at all the periods of the study, and liver - at days 10 and 15. Triterpenoid weakened cell depletion of bone marrow, thymus and limited hyperplasia of spleen compared with animals of groups II and III. Its protective effect did not correlate with increase of antibody titers. CONCLUSION: Miliacin weakens the severity of salmonellosis infection course.

[The development of secondary immunodeficiency in body when exposed to the effect of xenobiotics with immunosuppressive activity].

The State Education Institution of Higher professional education "The Orenburg State Medical Academy of Federal Agency in Public Health and Social Development". In the experiment on mice (CBA x C57Bl6) F1 and Wistar rats is shown the protective effect of triterpenoid plant--miliatsina (3-beta-methoxy-delta18-oleanena) in relation to the humoral immune response and clearance macrophage function hepatic xenobiotic conditions of use--methotrexate. The results define the term as used miliatsina immunoprotector with adverse effects on the body of environmental and industrial chemical factors that form the secondary immunodeficiency.

Triterpenoid miliacin inhibits stress-induced lipid peroxidation.

A plant triterpenoid miliacin prevented stress-induced activation of LPO and accumulation of LPO products in the blood. The inhibitory effect of miliacin was not related to direct inhibition of reactive oxygen species generation.

Effect of the triterpenoid miliacin on the sensitivity of lymphocytes in the thymus and spleen to dexamethasone-induced apoptosis.

We studied the effect of plant triterpenoid miliacin on dexamethasone-induced apoptosis in thymocytes and splenocytes. Miliacin produced a protective effect on splenocytes by decreasing the degree of DNA fragmentation due to blockade of the cascade cell death distally to the intramembrane phosphatidylserine translocation.