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Scientific Journal of Kurdistan University of Medical Science. 2018; 23 (3): 1-9
en Inglés, Persa | IMEMR | ID: emr-206663

RESUMEN

Background and Aim: Atherosclerosis is known as a multifactorial inflammatory disease. Trimethylamine N-oxide [TMAO] as a risk factor, has a potential to trigger or enhance the immune inflammatory reactions in atherosclerosis. Yet, The exact mechanism by which TMAO induces inflammation during atherosclerosis is not well understood. The present study was designed to evaluate the expression of IL-1 beta, IL-6, and TNF- alpha mRNA in response to treatment of macrophages with different concentrations of TMAO


Material andmethods: In this experimental in-vitro study, U937-derived macrophages were treated with different concentrations of TMAO [37.5, 75,150 and 300 micrometer] for 24 h. A group of cells were also treated with tunicamycin as positive control for stress. RT-qPCR was used to evaluate the expression of IL-1 beta, IL-6, and TNF- alpha mRNA levels. One-Way ANOVA and Post-hoc Dunnett test were used to compare the mean value of every group with that of control group


Results: Although TMAO increased expression of IL-1 beta, IL-6, and TNF- alpha mRNA, only 300 micrometer of TMAO significantly increased expression of IL-1 beta mRNA compared to the control cells [P<0.001]. Tunicamycin increased expression of IL-6 significantly


Conclusion: The results of this study showed that among the above mentioned cytokines, IL-1 beta as a proinflammatory cytokine had a greater role in inflammatory reactions, induced by TMAO as a risk factor for atherosclerosis

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