ArticleFrontiers in pharmacology2022
Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction by Inhibiting TLR4-NOX1/ROS Signaling Pathway in Caco-2 Cells.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- The central function and specific molecular mechanisms of the TLR4 pathway underlying impaired intestinal barrier in necrotizing enterocolitis.Biochemistry and biophysics reports · 2026Review
- Alisols A-C and their acetate derivatives: a review of natural occurrence, pharmacology, semisynthesis, pharmacokinetics, and metabolism.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Curcumin Attenuates LPS-Induced Migration/EMT and LPS/ATP-Associated IL-1β Release in Androgen-Independent Prostate Cancer Cells.Current issues in molecular biology · 2026Article
- Alisol B 23-acetate alleviates high-fat diet-induced insulin resistance by activating the SIRT1/FOXO1 axis and PI3K/AKT pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- C9orf72 Alleviates DSS‑Induced Ulcerative Colitis via the cGAS-STING Pathway.Immunity, inflammation and disease · 2025Article
- Article
- Review
- Review
- Protective effects and potential mechanisms of fermented egg-milk peptides on the damaged intestinal barrier.Frontiers in nutrition · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alisol B 23-Acetate (AB23A) is a naturally occurring triterpenoid, which can be indicated in the rhizome of medicinal and dietary plants from Alisma species. Previous studies have demonstrated that AB23A could inhibit intestinal permeability by regulating tight junction (TJ)-related proteins. Even so, the AB23A protective mechanism against intestinal barrier dysfunction remains poorly understood. This investigation seeks to evaluate the AB23A protective effects on intestinal barrier dysfunction and determine the mechanisms for restoring intestinal barrier dysfunction in LPS-stimulated Caco-2 monolayers. According to our findings, AB23A attenuated the inflammation by reducing pro-inflammatory cytokines production like IL-6, TNF-α, IL-1β, and prevented the paracellular permeability by inhibiting the disruption of TJ in LPS-induced Caco-2 monolayers after treated with LPS. AB23A also inhibited LPS-induced TLR4, NOX1 overexpression and subsequent ROS generation in Caco-2 monolayers. Transfected with NOX1-specific shRNA diminished the up-regulating AB23A effect on ZO-1 and occludin expression. Moreover, transfected with shRNA of TLR4 not only enhanced ZO-1 and occludin expression but attenuated NOX1 expression and ROS generation. Therefore, AB23A ameliorates LPS-induced intestinal barrier dysfunction by inhibiting TLR4-NOX1/ROS signaling pathway in Caco-2 monolayers, suggesting that AB23A may have positive impact on maintaining the intestinal barrier's integrity.
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