Effects of Dietary Pretreatment with All-trans Lycopene on Lipopolysaccharide-Induced Jejunal Inflammation: A Multi-Pathway Phenomenon

This study was conducted to investigate the effects and mechanisms of all-<i>trans</i> lycopene on intestinal health by establishing lipopolysaccharide-induced (LPS-induced) jejunal inflammation model. Dietary lycopene supplementation enhanced serum and jejunum antioxidant capacity. Lycopene significantly reduced LPS-induced upregulation of toll-like receptor-4 (TLR-4) and nuclear factor kappa-B (NF-κB), suggesting that lycopene reduced the activation of TLR-4/NF-κB signaling pathway induced by LPS challenge, and further protected mice from LPS induced jejunal inflammation. Furthermore, lycopene increased jejunal zonula occludens-1 (ZO-1) protein expression that was reduced by LPS challenge, and increased abundance of <i>Rikenella</i>, <i>Lachnospiraceae_NK4A136_group</i> and <i>Mucispirillum</i> potentially associated with reducing gut inflammation. Overall, these results showed that pretreatment with lycopene can improve jejunal inflammation and ensure intestinal health in mice by improving antioxidant capacity, intestinal barrier function, microorganisms potentially associated with anti-inflammatory effects and reducing the activation of TLR-4/NF-κB signaling pathway by LPS. We provided a new insight into lycopene prevented LPS-induced jejunal inflammation by corresponding alterations in serum metabolites and gut microbiota, improving antioxidant capacity and regulating the TLR-4/NF-κB signaling pathway in mice.

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Publication Details

Journal
Foods
Published
2025-02-26
DOI
https://doi.org/10.3390/foods14050794
Citations
3
Primary Topic
Antioxidant Activity and Oxidative Stress
Type
article
Field-Weighted Citation Impact
2.32
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article

Effects of Dietary Pretreatment with All-trans Lycopene on Lipopolysaccharide-Induced Jejunal Inflammation: A Multi-Pathway Phenomenon

Dajiang Ding, Daolin Mou, Junning Pu, Erhu Cao et al.
3 citations
Foods
Antioxidant Activity and Oxidative Stress
2.32
article

Effects of Dietary Pretreatment with All-trans Lycopene on Lipopolysaccharide-Induced Jejunal Inflammation: A Multi-Pathway Phenomenon

Dajiang Ding, Daolin Mou, Junning Pu, Erhu Cao, Wanxue Wen, Lu Ye, Xueyan Zhang, Ping Zhou, Jong-Liang Lan
article en
3 citations

Abstract

This study was conducted to investigate the effects and mechanisms of all-<i>trans</i> lycopene on intestinal health by establishing lipopolysaccharide-induced (LPS-induced) jejunal inflammation model. Dietary lycopene supplementation enhanced serum and jejunum antioxidant capacity. Lycopene significantly reduced LPS-induced upregulation of toll-like receptor-4 (TLR-4) and nuclear factor kappa-B (NF-κB), suggesting that lycopene reduced the activation of TLR-4/NF-κB signaling pathway induced by LPS challenge, and further protected mice from LPS induced jejunal inflammation. Furthermore, lycopene increased jejunal zonula occludens-1 (ZO-1) protein expression that was reduced by LPS challenge, and increased abundance of <i>Rikenella</i>, <i>Lachnospiraceae_NK4A136_group</i> and <i>Mucispirillum</i> potentially associated with reducing gut inflammation. Overall, these results showed that pretreatment with lycopene can improve jejunal inflammation and ensure intestinal health in mice by improving antioxidant capacity, intestinal barrier function, microorganisms potentially associated with anti-inflammatory effects and reducing the activation of TLR-4/NF-κB signaling pathway by LPS. We provided a new insight into lycopene prevented LPS-induced jejunal inflammation by corresponding alterations in serum metabolites and gut microbiota, improving antioxidant capacity and regulating the TLR-4/NF-κB signaling pathway in mice.

FoodsVol. 14(5)
Southwest University of Science and Technology (CN), Chinese Academy of Sciences (CN), Sichuan Agricultural University (CN), Center for Excellence in Brain Science and Intelligence Technology (CN), Sichuan University of Science and Engineering (CN)
Openalex Percentile: Top 13%
Antioxidant Activity and Oxidative Stress
2.32
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