Component

Mouse NF-kappa-B signaling readouts

6 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. Thymulin with equimolar zinc reduced I-kappa-B-alpha phosphorylation and p65 DNA binding in conditioned mouse macrophages.

    Thymulin → Mouse NF-kappa-B signaling readouts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Full text obtained; relevant results/methods inspected. This does not assert exhaustive figure/data reanalysis.
    experimental_condition
    Zinc-matched control peptide exposure · Thymulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Zinc-matched control equimolar zinc · Zinc(II) ion Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Thymulin plus equimolar zinc", "comparator": "Zinc-matched control", "endpoint": "Thymulin with equimolar zinc reduced I-kappa-B-alpha phosphorylation and p65 DNA binding in conditioned mouse macrophages.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "thymulin", "state": "peptide exposure"}, {"entity_slug": "zinc-ion", "state": "equimolar zinc"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse macrophages conditioned for one week, then challenged with LPS; human PBMC experiments used 24-hour pretreatment and are separate.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
    plain_language
    Thymulin with equimolar zinc reduced I-kappa-B-alpha phosphorylation and p65 DNA binding in conditioned mouse macrophages.
    primary_references
    Thymulin restrains age-associated myeloid inflammation and enhances cancer immunotherapy. | 2026 | DOI 10.1038/s41467-026-75383-0 | PMID 42481458 | https://www.nature.com/articles/s41467-026-75383-0
    source_locator
    Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 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 · Mouse macrophages conditioned for one week, then challenged with LPS; human PBMC experiments used 24-hour pretreatment and are separate. · Recorded from source · Recorded from source

    The 2026 Nature Communications study used **thymulin plus equimolar zinc versus zinc-matched controls**. Human PBMCs received 24-hour treatment before stimulated cytokine assessment. Mouse macrophages were conditioned during a week of differentiation, then challenged with LPS. Reduced IκBα phosphorylation, p65 DNA binding and inflammatory cytokine responses were reported. Mutation of an NF-κB site in an Il6 reporter removed the inhibitory reporter effect.
    Complete structured claim and evidence

  2. In mouse relapsing-remitting EAE, PBCA-thymulin altered p65 Ser276/JNK responses; later p65 Ser536 differences included a nonsignificant trend.

    PBCA nanoparticle-bound thymulin formulation → Mouse NF-kappa-B signaling readouts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Full text obtained; relevant results/methods inspected. This does not assert exhaustive figure/data reanalysis.
    experimental_contrast
    {"intervention": "PBCA-thymulin", "comparator": "Disease controls and free-peptide comparison", "endpoint": "In mouse relapsing-remitting EAE, PBCA-thymulin altered p65 Ser276/JNK responses; later p65 Ser536 differences included a nonsignificant trend.", "effect_direction": "mixed", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse EAE; formulation, phosphorylation site and day-dependent endpoints.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
    plain_language
    In mouse relapsing-remitting EAE, PBCA-thymulin altered p65 Ser276/JNK responses; later p65 Ser536 differences included a nonsignificant trend.
    primary_references
    Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice | 2019 | DOI 10.3390/ijms20215374 | PMID 31671728 | https://doi.org/10.3390/ijms20215374
    source_locator
    Reviewed reference lines 72-72; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 October 2026) · lines 72–72

    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 · Mouse EAE; formulation, phosphorylation site and day-dependent endpoints. · Recorded from source · Recorded from source

    | Relapsing-remitting experimental autoimmune encephalomyelitis in mice | PBCA-bound thymulin altered inflammatory signaling, including p65 Ser276 and JNK responses, with some effects persisting longer than free peptide. | Phosphorylation site and sampling day mattered; later p65 Ser536 differences included a nonsignificant trend. The measured p53 pathway did not respond. This is not demonstrated human multiple-sclerosis treatment. [2019 experiment](https://doi.org/10.3390/ijms20215374) |
    Complete structured claim and evidence

  3. In repeated-LPS mice, free thymulin reduced reported splenic nfkb phosphorylation/signaling readouts.

    Thymulin → Mouse NF-kappa-B signaling readouts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Full text obtained; relevant results/methods inspected. This does not assert exhaustive figure/data reanalysis.
    experimental_condition
    Repeated-LPS control tested formulation · Thymulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "thymulin with repeated LPS", "comparator": "Repeated-LPS control", "endpoint": "In repeated-LPS mice, free thymulin reduced reported splenic nfkb phosphorylation/signaling readouts.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "thymulin", "state": "tested formulation"}, {"entity_slug": null, "state": "repeated LPS"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Repeated-LPS mouse model; not human infectious sepsis. Free and nanoparticle formulations are separate.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
    plain_language
    In repeated-LPS mice, free thymulin reduced reported splenic nfkb phosphorylation/signaling readouts.
    primary_references
    Thymulin, free or bound to PBCA nanoparticles, protects mice against chronic septic inflammation | 2018 | DOI 10.1371/journal.pone.0197601 | PMID 29795607 | https://doi.org/10.1371/journal.pone.0197601
    source_locator
    Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 October 2026) · lines 71–71

    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 · Repeated-LPS mouse model; not human infectious sepsis. Free and nanoparticle formulations are separate. · Recorded from source · Recorded from source

    | Mice receiving repeated LPS, free thymulin or PBCA-bound thymulin | Reduced splenic phosphorylation of IKK, p65, JNK, p38 and PKCθ was reported, with changes in stress proteins and apoptosis-related readouts. | Repeated endotoxin exposure is not the same as human infectious sepsis. Free peptide and nanoparticle formulations require separate exposure records. [2018 experiment](https://doi.org/10.1371/journal.pone.0197601) |
    Complete structured claim and evidence

  4. In repeated-LPS mice, PBCA-bound thymulin reduced reported splenic nfkb phosphorylation/signaling readouts.

    PBCA nanoparticle-bound thymulin formulation → Mouse NF-kappa-B signaling readouts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Full text obtained; relevant results/methods inspected. This does not assert exhaustive figure/data reanalysis.
    experimental_condition
    Repeated-LPS control tested formulation · PBCA nanoparticle-bound thymulin formulation Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "pbca-thymulin with repeated LPS", "comparator": "Repeated-LPS control", "endpoint": "In repeated-LPS mice, PBCA-bound thymulin reduced reported splenic nfkb phosphorylation/signaling readouts.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "pbca-thymulin", "state": "tested formulation"}, {"entity_slug": null, "state": "repeated LPS"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Repeated-LPS mouse model; not human infectious sepsis. Free and nanoparticle formulations are separate.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
    plain_language
    In repeated-LPS mice, PBCA-bound thymulin reduced reported splenic nfkb phosphorylation/signaling readouts.
    primary_references
    Thymulin, free or bound to PBCA nanoparticles, protects mice against chronic septic inflammation | 2018 | DOI 10.1371/journal.pone.0197601 | PMID 29795607 | https://doi.org/10.1371/journal.pone.0197601
    source_locator
    Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 October 2026) · lines 71–71

    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 · Repeated-LPS mouse model; not human infectious sepsis. Free and nanoparticle formulations are separate. · Recorded from source · Recorded from source

    | Mice receiving repeated LPS, free thymulin or PBCA-bound thymulin | Reduced splenic phosphorylation of IKK, p65, JNK, p38 and PKCθ was reported, with changes in stress proteins and apoptosis-related readouts. | Repeated endotoxin exposure is not the same as human infectious sepsis. Free peptide and nanoparticle formulations require separate exposure records. [2018 experiment](https://doi.org/10.1371/journal.pone.0197601) |
    Complete structured claim and evidence

  5. Thymulin did not reduce the reported NF-kappa-B activation readout in LPS-stimulated RAW264.7 macrophages; this is not evidence for unconditional NF-kappa-B inhibition.

    Thymulin → Mouse NF-kappa-B signaling readouts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary bibliographic record and abstract checked; full methods/figures not comprehensively reviewed.
    experimental_condition
    LPS alone added peptide · Thymulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Thymulin plus LPS", "comparator": "LPS alone", "endpoint": "Thymulin did not reduce the reported NF-kappa-B activation readout in LPS-stimulated RAW264.7 macrophages; this is not evidence for unconditional NF-kappa-B inhibition.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "thymulin", "state": "added peptide"}, {"entity_slug": null, "state": "LPS stimulation"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse RAW264.7 macrophages; LPS stimulation; endpoint retained at reported pathway level.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
    plain_language
    Thymulin did not reduce the reported NF-kappa-B activation readout in LPS-stimulated RAW264.7 macrophages; this is not evidence for unconditional NF-kappa-B inhibition.
    primary_references
    Thymus peptides regulate activity of RAW 264.7 macrophage cells: inhibitory analysis and a role of signal cascades. | 2011 | DOI 10.1517/14728222.2011.641952 | PMID 22148922 | https://pubmed.ncbi.nlm.nih.gov/22148922/
    source_locator
    Reviewed reference lines 68-68; exact primary location described in quoted passage where extracted.

    Thymulin: detailed mechanisms of action (reviewed 3 October 2026) · lines 68–68

    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 · Mouse RAW264.7 macrophages; LPS stimulation; endpoint retained at reported pathway level. · Recorded from source · Recorded from source

    | RAW264.7 macrophages, unstimulated versus LPS-stimulated | In resting cells, thymulin increased proinflammatory cytokine secretion. In LPS-stimulated cells, it reduced SAPK/JNK activity but not NF-κB activity; peptide alone did not change the measured cytokine secretion. HSP72 increased. | Preserve the resting/stimulated contrast. Thymopentin was also studied and requires separate attribution. [2011 experiment](https://pubmed.ncbi.nlm.nih.gov/22148922/) |
    Complete structured claim and evidence

  6. RA was associated with reduced NF-kappa-B signaling in the bacterial-challenge mouse and epithelial-cell experiments.

    Rosmarinic acid → Mouse NF-kappa-B signaling readouts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    experimental_contrast
    {"intervention": "RA pretreatment plus E. coli challenge", "comparator": "E. coli challenge alone", "endpoint": "RA was associated with reduced NF-kappa-B signaling in the bacterial-challenge mouse and epithelial-cell experiments.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    Mouse gavage 20 mg/kg for one week; accompanying epithelial-cell pretreatment 6 h and bacterial challenge 3 h.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Rosmarinic acid collection; exact intervention and molecular form govern interpretation. · Rosmarinic acid
    plain_language
    RA was associated with reduced NF-kappa-B signaling in the bacterial-challenge mouse and epithelial-cell experiments.
    primary_references
    Rosmarinic acid alleviated intestinal barrier damage caused by <i>Escherichia coli</i> by regulating the gut microbiota and inhibiting the NF-κB signalling pathway in mice. | https://pubmed.ncbi.nlm.nih.gov/39540591/ | https://doi.org/10.1039/d4fo02654c
    source_locator
    Reviewed reference ra-mouse-inflammatory-signaling; Primary abstract; exact subunit and direct binding were not established.

    Rosmarinic acid: detailed mechanisms of action (reviewed 10 October 2026) · lines 606–612

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse gavage 20 mg/kg for one week; accompanying epithelial-cell pretreatment 6 h and bacterial challenge 3 h. · Recorded from source · Recorded from source

    ### ra-mouse-inflammatory-signaling RA was associated with reduced NF-kappa-B signaling in the bacterial-challenge mouse and epithelial-cell experiments. Primary abstract; exact subunit and direct binding were not established. Model and exposure: Mouse gavage 20 mg/kg for one week; accompanying epithelial-cell pretreatment 6 h and bacterial challenge 3 h. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Rosmarinic acid alleviated intestinal barrier damage caused by <i>Escherichia coli</i> by regulating the gut microbiota and inhibiting the NF-κB signalling pathway in mice. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39540591/ | https://doi.org/10.1039/d4fo02654c | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
    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.