Component
Human NADPH oxidase 1 / NOX1
Context-specific entity; species, compartment and exposure are stated on each claim.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Ergothioneine decreased NOX1 expression in the human endothelial-cell study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human brain microvascular endothelial cells.
- limitations
- Expression change, not demonstrated direct NOX1 inhibition.
- nutrient_topic
- Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine
- plain_language
- The response included a lower oxidant-generating enzyme signal.
- primary_references
- Uptake and protective effects of ergothioneine in human endothelial cells. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25022513/ · DOI 10.1124/jpet.114.214049
Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 288–294
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human brain microvascular endothelial cells. · source_derived_draft · unverified_draft
## ergothioneine-endothelial-nox1 The response included a lower oxidant-generating enzyme signal. Ergothioneine decreased NOX1 expression in the human endothelial-cell study. Model: Human brain microvascular endothelial cells. Limitations: Expression change, not demonstrated direct NOX1 inhibition. Evidence access: Primary abstract Uptake and protective effects of ergothioneine in human endothelial cells. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25022513/ · DOI 10.1124/jpet.114.214049
Complete structured claim and evidenceIndicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.
Experimental context and source evidence
- dose
- Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
- duration
- 24 h for mediator release and permeability; earlier signaling assays
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Differentiated human Caco-2 intestinal epithelial monolayers
- limitations
- No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Differentiated human Caco-2 intestinal epithelial monolayers
- plain_language
- Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers.
- primary_references
- Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
- route
- In vitro co-incubation
- tissue
- Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 257–265
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-nox1 Indicaxanthin co-treatment prevented IL-1beta-induced NOX1 activation in Caco-2 monolayers. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
Where it participates (unsigned role)
Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.
Experimental context and source evidence
- dose
- Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL
- duration
- 24 h for mediator release and permeability; earlier signaling assays
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Differentiated human Caco-2 intestinal epithelial monolayers
- limitations
- No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Differentiated human Caco-2 intestinal epithelial monolayers
- plain_language
- Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal.
- primary_references
- Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
- route
- In vitro co-incubation
- tissue
- Intestinal epithelial model
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 297–305
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Differentiated human Caco-2 intestinal epithelial monolayers · source_derived_draft · unverified_draft
## betalains-caco2-ros Indicaxanthin prevented the IL-1beta-associated rise in cellular oxidant signal. Model/species: Differentiated human Caco-2 intestinal epithelial monolayers Tissue: Intestinal epithelial model Exposure: Indicaxanthin 5-25 micromolar with IL-1beta 25 ng/mL Route: In vitro co-incubation Duration: 24 h for mediator release and permeability; earlier signaling assays Limits: No clinical IBD treatment effect or molecular binding site was established. Total thiols must not be relabeled as a specific glutathione measurement. Primary reference: Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1β-exposed Caco-2 cells. (2014). https://pubmed.ncbi.nlm.nih.gov/23931157/ DOI: 10.1017/S0007114513002663
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.