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. 2021 Jan 7;18:6. doi: 10.1186/s12986-020-00535-y

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Plasma levels of TMAO, inflammatory cytokines, and oxidative stress-related parameters in ApoE^−/− mice. a Plasma level of TMAO. The inflammatory cytokines include b tumor necrosis factor α (TNF-α), c interleukin (IL)-1β, d IL-6, e monocyte chemoattractant protein 1 (MCP-1), and f IL-10. Plasma levels of g total antioxidant capacity (T-AOC), h superoxide dismutase (SOD) activity, i glutathione peroxidase (GSH-Px) activity, and j malondialdehyde (MDA) in ApoE^−/− mice. Data are expressed as mean with SD, n = 8. ^a,b,cmeans with different superscript letters differ significantly at p < 0.05 by one-way ANOVA. p for dose effect was analyzed using ordinary linear regression across WD + TMAO, WD + TMAO + L-HFE, and WD + TMAO + H-HFE groups