Effects of Dietary Pretreatment with All-<i>trans</i> 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. Lyco...

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Main Authors: Daolin Mou, Dajiang Ding, Junning Pu, Pan Zhou, Enming Cao, Xueyan Zhang, Junrong Lan, Lu Ye, Wanxue Wen
Format: Article
Language:English
Published: MDPI AG 2025-02-01
Series:Foods
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Online Access:https://www.mdpi.com/2304-8158/14/5/794
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Summary: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.
ISSN:2304-8158