Regulatory effects of flavonoids luteolin on BDE-209-induced intestinal epithelial barrier damage in Caco-2 cell monolayer model

Yuan, Jinwen; Che, Siyan; Ruan, Zheng; Song, Luqing; Tang, Rongxue; Zhang, Li

doi:10.1016/j.fct.2021.112098

Cited by 34 publications

(24 citation statements)

References 41 publications

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“…These results indicated that SEA exposure induced intestinal-barrier dysfunction in mice, which might lead to harmful substances entering the immune system and trigger an inflammatory response. Therefore, the development of compounds to restore intestinal barrier function may be a promising strategy for the prevention and treatment of SEA-caused foodborne diseases [16,24,29].…”

Section: Discussionmentioning

confidence: 99%

“…The activation of the MAPK pathway involves the phosphorylation of JNK, ERK and p38, which regulates the expression of inflammatory genes [31,42]. Importantly, the MAPK signaling pathway has been proved to regulate intestinal TJ proteins [24]. Increasing evidence has indicated that the NF-κB and MAPK signaling pathways have played a crucial role in the pathogenesis of intestinal inflammation and NLRP3 inflammasome activation.…”

Section: Discussionmentioning

confidence: 99%

“…As the key signaling pathways of various inflammatory diseases, the activation of NF-κB and MAPK promotes the secretion of proinflammatory cytokines, resulting in an inflammatory response [22]. Moreover, as the important signal transduction and transcription factors, NF-κB and MAPK pathways were confirmed to regulate the expression of TJ proteins, which was vital to the actin contraction and to mucosal barrier damage [23,24]. Therefore, NF-κB/MAPK mediated activation of NLRP3 inflammasome is an important mechanism of intestinal barrier dysfunction and inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

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Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Liu

Chi

Yang

et al. 2022

Toxins

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Staphylococcal enterotoxin A (SEA), the toxin protein secreted by Staphylococcus aureus, can cause staphylococcal food poisoning outbreaks and seriously threaten global public health. However, little is known about the pathogenesis of SEA in staphylococcal foodborne diseases. In this study, the effect of SEA on intestinal barrier injury and NLRP3 inflammasome activation was investigated by exposing BALB/c mice to SEA with increasing doses and a potential toxic mechanism was elucidated. Our findings suggested that SEA exposure provoked villi injury and suppressed the expression of ZO-1 and occludin proteins, thereby inducing intestinal barrier dysfunction and small intestinal injury in mice. Concurrently, SEA significantly up-regulated the expression of NLRP3 inflammasome-associated proteins and triggered the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways in jejunum tissues. Notably, selective inhibitors of MAPKs and NF-κB p65 ameliorated the activation of NLRP3 inflammasome stimulated by SEA, which further indicated that SEA could activate NLRP3 inflammasome through NF-κB/MAPK pathways. In summary, SEA was first confirmed to induce intestinal barrier dysfunction and activate NLRP3 inflammasome via NF-κB/MAPK signaling pathways. These findings will contribute to a more comprehensive understanding of the pathogenesis of SEA and related drug-screening for the treatment and prevention of bacteriotoxin-caused foodborne diseases via targeting specific pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Liu

Chi

Yang

et al. 2022

Toxins

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“…Luteolin is a kind of flavonoid and studies about its effects on lipid metabolism disorder and intestinal flora composition in rats fed a high-fat diet shows that luteolin combined with metformin hydrochloride can decrease the proportion of Firmicute and Bacteroidetes (F/ B), to increase the relative abundance of Lachnospiraceae, Helicobacteraceae, algae, and Peptococcaceae as well as alleviate lipid metabolism disorder and optimize the composition of intestinal flora in high-fat diet rats. In addition, luteolin can enhance the intestinal barrier by decreasing the level of reactive oxygen species (ROS), increasing the activity of superoxide dismutase (SOD) and glutathione (GSH), and inhibiting the secretion of proinflammatory cytokines [26,27]. Kaempferol is a natural flavanol with multiple pharmacological activities.…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology Analysis of Xuanfei Baidu Granule in the Treatment of Intestinal Flora Disorder

Miao

Chen

Zhang

et al. 2022

Advanced Gut & Microbiome Research

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Objective. This study is aimed at analyzing the molecular mechanism of Xuanfei Baidu Granule (XFBDG) in the treatment of intestinal flora disorder based on network pharmacology. Methods. The TCMSP database was used to obtain the active components and target proteins of XFBDG, while the GeneCards database was used to obtain the related proteins of intestinal flora disorder. The Rx64 4.0.2 software was used to analyze the GO functional enrichment and KEGG pathway enrichment of drug component target protein and disease-related protein to obtain the pathway-enriched proteins and screen the core proteins for topology analysis of the pathway target by using the STRING database and Cytoscape v3.8.2 software. The Cytoscape v3.8.2 software was used to analyze the relationship between each component and enriched protein, and the AutoDock Vina software was used for molecular docking of core proteins and components. Results. XFBDG contains 133 active components that can act on 249 proteins related to intestinal flora disorder. The effects include the following: (i) regulation of functions—the response to drug, cellular response to chemical stress, response to oxidative stress, and RNA polymerase II-specific DNA-binding transcription factor binding and (ii) regulation of signaling pathways such as the IL-17 signaling pathway, TNF signaling pathway, and Th17 cell differentiation pathway. The enriched core proteins in these pathways are IFNG, IL4, PTGS2, JUN, and IL1B that set in a higher level of binding with the corresponding drug components. Conclusion. XFBDG can act on IFNG, IL4, PTGS2, JUN, and IL1B proteins through its active components such as quercetin, luteolin, and kaempferol to regulate the IL-17, TNF, and Th17 cell differentiation pathways and further regulate the response to drug, cellular response to chemical stress, response to oxidative stress, and RNA polymerase II-specific DNA-binding transcription factor binding. In addition, owing to its antioxidant and anti-inflammatory properties and related immune responses, XFBDG can achieve a balance of intestinal flora and microbial metabolism.

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“…More specifically, luteolin can attenuate ulcerative colitis, suppress rectal cancer, and prevent irinotecan-induced mucositis [104][105][106][107]. From another perspective, luteolin had a notably alleviative effect on intestinal barrier damage induced by decabromodiphenyl ether (BDE-209) in a Caco-2 cell monolayer model through suppressing the phosphorylation of IκBα and the accumulation of NF-κB p50 and ERK expression [42]. Luteolin also relieved DSS-induced colitis in mice, and the mechanism by which is due to the suppression of high mobility group box chromosomal 1 (HMGB1), TLR4, and NF-κB p65 protein levels in the colon [43].…”

Section: Luteolinmentioning

confidence: 99%

Pharmacological Effects of Polyphenol Phytochemicals on the Intestinal Inflammation via Targeting TLR4/NF-κB Signaling Pathway

Wang

Yang

2022

IJMS

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TLR4/NF-κB is a key inflammatory signaling transduction pathway, closely involved in cell differentiation, proliferation, apoptosis, and pro-inflammatory response. Toll like receptor 4 (TLR4), the first mammalian TLR to be characterized, is the innate immune receptor that plays a key role in inflammatory signal transductions. Nuclear factor kappa B (NF-κB), the TLR4 downstream, is the key to accounting for the expression of multiple genes involved in inflammatory responses, such as pro-inflammatory cytokines. Inflammatory bowel disease (IBD) in humans is a chronic inflammatory disease with high incidence and prevalence worldwide. Targeting the TLR4/NF-κB signaling pathway might be an effective strategy to alleviate intestinal inflammation. Polyphenol phytochemicals have shown noticeable alleviative effects by acting on the TLR4/NF-κB signaling pathway in intestinal inflammation. This review summarizes the pharmacological effects of more than 20 kinds of polyphenols on intestinal inflammation via targeting the TLR4/NF-κB signaling pathway. We expected that polyphenol phytochemicals targeting the TLR4/NF-κB signaling pathway might be an effective approach to treat IBD in future clinical research applications.

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Regulatory effects of flavonoids luteolin on BDE-209-induced intestinal epithelial barrier damage in Caco-2 cell monolayer model

Cited by 34 publications

References 41 publications

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Network Pharmacology Analysis of Xuanfei Baidu Granule in the Treatment of Intestinal Flora Disorder

Pharmacological Effects of Polyphenol Phytochemicals on the Intestinal Inflammation via Targeting TLR4/NF-κB Signaling Pathway

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