Cited by 110Flavonoids in Medical ResearchGastrointestinal motility and disordersBarrier Structure and Function Studies

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Wogonin suppresses inflammatory response and maintains intestinal barrier function via TLR4-MyD88-TAK1-mediated NF-κB pathway in vitro

Wang, Wenping, Xia, Tingsong, Yu, Xinpu·2015·Inflammation Research

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Abstract

Aims and objective Wogonin has multiple pharmacological effects, including anti-inflammatory effects. Here, we hypothesize that wogonin can protect intestinal barrier function in lipopolysaccharide (LPS)-induced Caco-2 cells, which is an in vitro model of intestinal inflammation.Methods We measured intestinal barrier function in LPS-induced Caco-2 cells by using transepithelial electrical resistance (TEER) and transport of fluorescent markers. A quantitative (q) RT-PCR and immunofluorescent staining analysis was used to detect the expression of tight junction proteins (claudin-1 and ZO-1) in LPS-induced Caco-2 cells. We measured inflammatory molecules in LPS-induced Caco-2 cells using ELISA and qRT-PCR. In addition, the expression of TLR4, MyD88 and TAK1 and their interaction, and NF-κB activity in LPS-induced Caco-2 cells were investigated by western blot analysis and immune-precipitation.Results We found that exposing Caco-2 cells to wogonin (10 and 50 μM for 24 h) attenuated the LPS-induced changes in TEER and transport of fluorescent markers. In addition, wogonin suppressed LPS-induced down-regulation of tight junction proteins (claudin-1 and ZO-1). Furthermore, LPS-induced up-regulation of inflammatory mediators, including interleukin (IL)-1β, IL-6 and IL-8, cyclooxygenase-2 (COX-2), inducible nitric oxide synthases (iNOS) were reduced after being pre-treated with wogonin. Moreover, wogonin not only inhibited the expression of TLR4, MyD88 and TAK1 and the interaction between these molecules, but also reduced NF-κB translocation to nucleus and its DNA-binding activity in LPS-induced Caco-2 cells.Conclusion Our results suggested that pre-treatment with wogonin could attenuate the TLR4-mediated inflammatory response and maintain intestinal barrier function in LPS-induced Caco-2 cells, thus might be a potential therapy for treating IBD.

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Authors: Wang, W., Xia, T., & Yu, X.
Affiliations: Jiangyin People's Hospital (CN)
ORCID: Wang, Wenping
Venue: Inflammation Research
Publisher: Springer Science and Business Media LLC
Published: 2015-04-28
Volume: 64
Issue: 6
Pages: 423-431
ISSN: 1023-3830 (ISSN-L)
1420-908X
DOI: 10.1007/s00011-015-0822-0
OpenAlex: W2079479624
Cited by: 110
References: 27
Citations by year: 2026: 8 · 2025: 10 · 2024: 9 · 2023: 10 · 2022: 14 · 2021: 9 · 2020: 9 · 2019: 5 · 2018: 9 · 2017: 13 · 2016: 12 · 2015: 2
FWCI: 8.69
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Inflammation Research (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pharmacology (medical) › Flavonoids in Medical Research
Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Keywords: wogonin, intestinal barrier function, intestinal inflammation, TLR4, MyD88, TAK1, NF-κB signaling, lipopolysaccharide, Caco-2 cells, tight junction proteins, claudin-1, ZO-1, inflammatory cytokines, cyclooxygenase-2, inducible nitric oxide synthase, inflammatory bowel disease
MeSH terms: MAP Kinase Kinase Kinase 7, Anti-Inflammatory Agents, Antioxidants, Biological Transport, Active, Humans, Interleukins, Intestines, Signal Transduction, NF-kappa B, Electric Impedance, Inflammation Mediators, Caco-2 Cells, MAP Kinase Kinase Kinases, Flavanones, Toll-Like Receptor 4, Myeloid Differentiation Factor 88, Claudin-1

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Wogonin suppresses inflammatory response and maintains intestinal barrier function via TLR4-MyD88-TAK1-mediated NF-κB pathway in vitro

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