Component

Human Caco-2 paracellular permeability and electrical resistance

Human Caco-2 paracellular permeability and electrical resistance. Interpret through the linked experimental species, preparation, compartment and exposure; no universal causal effect is implied.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.

    Cyanidin 3-O-beta-D-glucopyranoside → Human Caco-2 paracellular permeability and electrical resistance source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
    experimental_condition
    TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    TNF without test glucoside present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "cyanidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
    plain_language
    cyanidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.
    primary_references
    Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
    source_locator
    Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · source_derived_draft · unverified_draft

    **Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
    Complete structured claim and evidence

  2. delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.

    Delphinidin 3-O-beta-D-glucopyranoside → Human Caco-2 paracellular permeability and electrical resistance source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
    experimental_condition
    TNF without test glucoside present · Delphinidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "delphinidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "delphinidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
    plain_language
    delphinidin-3-glucoside limited TNF-induced barrier permeability, measured by electrical resistance and FITC-dextran flux.
    primary_references
    Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
    source_locator
    Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · source_derived_draft · unverified_draft

    **Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
    Complete structured claim and evidence

  3. malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.

    Malvidin 3-O-glucoside → Human Caco-2 paracellular permeability and electrical resistance source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
    experimental_condition
    TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    TNF without test glucoside present · Malvidin 3-O-glucoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "malvidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "malvidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
    plain_language
    malvidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
    primary_references
    Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
    source_locator
    Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · source_derived_draft · unverified_draft

    **Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
    Complete structured claim and evidence

  4. peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.

    Peonidin 3-O-glucoside → Human Caco-2 paracellular permeability and electrical resistance source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
    experimental_condition
    TNF without test glucoside present · Peonidin 3-O-glucoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "peonidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "peonidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
    plain_language
    peonidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
    primary_references
    Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
    source_locator
    Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · source_derived_draft · unverified_draft

    **Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
    Complete structured claim and evidence

  5. petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.

    Petunidin 3-O-glucoside → Human Caco-2 paracellular permeability and electrical resistance source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.
    experimental_condition
    TNF without test glucoside present · Tumor necrosis factor Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    TNF without test glucoside present · Petunidin 3-O-glucoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "petunidin-3-glucoside plus TNF", "comparator": "TNF without test glucoside", "endpoint": "petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "petunidin-3-glucoside", "state": "present"}, {"entity_slug": "tnf", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Not generic class activity or clinical gut-disease treatment. Electrical resistance and tracer flux have opposite directions; claim direction describes permeability.
    plain_language
    petunidin-3-glucoside did not show the same protection against TNF-induced barrier permeability in the tested concentration range.
    primary_references
    Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j
    source_locator
    Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 78–78

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Differentiated human Caco-2, 0.25-1 uM O-glucoside, TNF challenge; functional TEER and FITC-dextran readouts. · source_derived_draft · unverified_draft

    **Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.