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-1β, IL-6, and TNF-α mRNA in response to treatment of macrophages with different concentrations of TMAO.

Material and Methods: In this experimental in-vitro study, U937-derived macrophages were treated with different concentrations of TMAO (37.5, 75,150 and 300 µM) 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-1β, IL-6, and TNF-α 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-1β, IL-6, and TNF-α mRNA, only 300 µM of TMAO significantly increased expression of IL-1β 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-1β as a proinflammatory cytokine had a greater role in inflammatory reactions, induced by TMAO as a risk factor for atherosclerosis.

Keywords: Cytokine, Atherosclerosis, Trimethylamine-N-Oxide, Tunicamycin, Macrophage.

Received: Nov 21, 2017     Accepted: May 15, 2018