Wogonin suppresses inflammatory response and maintains intestinal barrier function via TLR4-MyD88-TAK1-mediated NF-κB pathway in vitro
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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Wogonin suppresses the inflammatory response and maintains intestinal barrier function via the TLR4-MyD88-TAK1-NF-κB pathway in Caco-2 cells.
“For example, wogonin suppresses the inflammatory response and maintains intestinal barrier function via the TLR4-MyD88-TAK1 (TGF-β activated kinase 1)-NF-κB (nuclear factor-kappa B) pathway in Caco-2 cells.160”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [160]
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- Authors
- Wang, W., Xia, T., & Yu, X.
- Affiliations
- Jiangyin People's Hospital (CN)
- ORCID
- Wang, Wenping
- Venue
- Inflammation Research
- Published
- 2015-04-28
- Volume
- 64
- Issue
- 6
- Pages
- 423-431
- ISSN
- 1023-3830 (ISSN-L)
- 1420-908X
- 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 › 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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