Abstract

By infection Toxoplasma gondii (T.gondii) caused Toxoplasmosis is a serious zoonoses disease and opportunistic, and often causes serious risk of life in patients who are immunocompromised. Toxoplasmosis is a serious zoonoses disease and opportunistic, and often causes serious risk of life in patients who are immunocompromised. Dexamethasone (DEX) is widely used in the clinic for inflammatory, autoimmune of treatment. However, long-term use of DEX is often easy to lead to acute toxoplasmosis in patients, and the potential molecular mechanism is still not very clear. The aims of this study were to investigate the effect of DEX on proliferation of Toxoplasma and its molecular mechanisms, and to establish the corresponding control measures. All the results showed that dexamethasone could enhance the proliferation of the Toxoplasma gondii (T.gondii) tachyzoites. After 72h, 566 (±7) tachyzoites were found in 100 host cells, while only 86 (±8) tachyzoites were counted from the non-treated control cells (P <0.01). Gas chromatography analysis showed obvious changes in the number and composition of fatty acids in DEX-treated host cells and T.gondii. Analysis showed the fatty acids C16:0 showed a decrease from 22.987 to 18.381, and fatty acids C18:1 increased from 2.402 to 4.335, after being in the DEX-treated T.gondii. Gas chromatography analysis showed the fatty acids C18:1 increase from 5.099 to 8.628, and fatty acids C16:0 showed an decrease from 7.281 to 6.549, after being in the DEX-treated RAW-264 cells. We evaluate the effects of dexamethasone treated on plasma polyunsaturated fatty acids in mice, and showed the fatty acids C18:1 increase from 5.326 to 14.630. Fish oil was added as a modulator of lipid metabolism in experimental mice. It was found that mice fed with fish oil did not develop the disease after infection with T.gondii, and the structure of fatty acids in plasma changed significantly. Fish oil was added as a modulator of lipid metabolism in experimental mice. Fish oil supplementation increased C22:6 (DEX: 2.622±0.01%; DFT: 15.455±0.01%) and C20:4 (DEX: 2.627±0.01%; DFT: 3.073±0.01%) contents and decrease the C18:1(DEX: 14.630±0.01%; DFT: 4.513±0.01%) in DFT mice compared with DEX mice. These results indicate that the molecular mechanism of dexamethasone to

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