Component
NF-kappaB family
Independent biological entity. Read linked claims for experimental scope and context.
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
Benfotiamine inhibited hyperglycemia-associated NF-kappaB activation in the tested models.
Experimental context and source evidence
- experimental_model
- High-glucose bovine endothelial cells and diabetic rat retinal experiments.
- exposure
- Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
- limitations
- Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Bos taurus; Rattus norvegicus
- plain_language
- An inflammatory signaling readout also declined in these experiments.
- primary_references
- [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
- tissue_or_cell_type
- Endothelial cultures and retina
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1927–1937
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft
### b1-benfotiamine-nfkb Benfotiamine inhibited hyperglycemia-associated NF-kappaB activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory signaling readout also declined in these experiments. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
Complete structured claim and evidence
Where it participates (unsigned role)
Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs.
Experimental context and source evidence
- dose
- Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL
- duration
- 1 h pretreatment followed by 16 h oxidized-LDL exposure
- evidence_access
- Primary open full text, relevant results/methods and PubMed metadata.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- Human umbilical vein endothelial cells / HUVECs
- limitations
- Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed.
- nutrient_topic
- Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
- organism
- Human umbilical vein endothelial cells / HUVECs
- plain_language
- Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs.
- primary_references
- Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846
- route
- In vitro pretreatment and challenge
- tissue
- Endothelial culture
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 338–347
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human umbilical vein endothelial cells / HUVECs · source_derived_draft · unverified_draft
## indicaxanthin-endothelial-nfkb Indicaxanthin pretreatment suppressed oxidized-LDL-induced NF-kappaB transcriptional activity in HUVECs. Model/species: Human umbilical vein endothelial cells / HUVECs Tissue: Endothelial culture Exposure: Indicaxanthin 5-20 micromolar; human oxidized LDL 100 micrograms/mL Route: In vitro pretreatment and challenge Duration: 1 h pretreatment followed by 16 h oxidized-LDL exposure Limits: Expression rescue does not demonstrate plaque regression or ABCA1 cholesterol-efflux flux. Primary-source metadata check found no correction/retraction link; broader integrity not assessed. Primary reference: Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation. (2019). https://pubmed.ncbi.nlm.nih.gov/30911345/ DOI: 10.1155/2019/3457846 Access: Primary open full text, relevant results/methods and PubMed metadata.
Complete structured claim and evidenceIndicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation.
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 suppressed IL-1beta-induced NF-kappaB activation.
- 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 267–275
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-nfkb Indicaxanthin co-treatment suppressed IL-1beta-induced NF-kappaB activation. 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.