Gut Microbiota Derived Trimethylamine-N-Oxide (TMAO) Prompts Atherosclerosis Via the Expression of TLR2 and NADPH Oxidase

  • سال انتشار: 1397
  • محل انتشار: سومین کنگره بین المللی پزشکی شخصی ایران
  • کد COI اختصاصی: IPMCMED03_122
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 573
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نویسندگان

Abbas Ahmadi

Cellular and Molecular Research Center, Research Institute for Health Development, Department of Molecular Medicine and Genetics, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran

Zakaria Vahabzadeh

Liver and Digestive Research Center, Department of Clinical Biochemistry, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran

چکیده

Background: Gut microbiota-dependent metabolites, especially trimethylamine N-oxide (TMAO), have lately been proposed to induce atherosclerosis. However, the exact mechanism is not well understood. Commitment of macrophages toll-like receptors (TLRs) and consequently their downstream NADPH oxidases (NOX) activate the signaling pathways that initiate pro-inflammatory cytokines as well as ROS production. The present study was designed to evaluate the expression of TLR2, TLR6 and NOX2 in macrophages.Methods: Macrophages cell lines (U937 and THP-1) were treated with different concentration of TMAO (37.5, 75, 150 and 300 μM) for 24 h. The cells were also treated with Tunicamycin (TN), as a positive control. RT-qPCR was used to evaluate the expression of TLR2, TLR6, and NOX2 at mRNA levels.Results: Unlike TN, high dose of TMAO significantly increased TLR2 and NOX2 mRNA levels compared to the control cells (p< 0.05). TN alone significantly increased the mRNA levels of TLR6 (p=0.010). Conclusion: Our findings provide positive evidence to support the influence of TLR2 and NOX2 in proatherogenic mechanism of TMAO during the foam cell formation and abnormal activation of macrophages.

کلیدواژه ها

Trimethylamine-N-Oxide, Atherosclerosis, Toll-like receptors, NADPH oxidase

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