Component

(+)-Lariciresinol

Dextrorotatory enantiomer; carries the macrophage antioxidant and antibacterial findings.

7 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 it acts on

  1. (+)-Lariciresinol activated p38 in murine macrophages.

    (+)-Lariciresinol → p38 mitogen-activated protein kinase family source_derived_draftungraded
    Experimental context and source evidence
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    RAW 264.7 murine macrophages
    exposure
    (+)-Lariciresinol isolated from Rubia philippinensis
    limitations
    The abstract states p38 activation without giving concentrations or timing; those appear only in the full text and figures and were not read here.
    organism
    RAW 264.7 murine macrophages
    plain_language
    (+)-Lariciresinol activated p38 in murine macrophages.
    primary_references
    Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035
    route
    In vitro
    tissue
    Mitogen-activated protein kinase phosphorylation

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 11–20

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## plus-lariciresinol-activates-p38 (+)-Lariciresinol activated p38 in murine macrophages. Model/species: RAW 264.7 murine macrophages Tissue/system: Mitogen-activated protein kinase phosphorylation Exposure: (+)-Lariciresinol isolated from Rubia philippinensis Route: In vitro Duration: Acute Limits: The abstract states p38 activation without giving concentrations or timing; those appear only in the full text and figures and were not read here. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. (+)-Lariciresinol inhibited reactive oxygen species generation in murine macrophages in a dose-dependent manner without cytotoxicity.

    (+)-Lariciresinol → Reactive oxygen species generation in RAW 264.7 macrophages source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    RAW 264.7 murine macrophages
    exposure
    (+)-Lariciresinol, dose-dependent
    limitations
    The abstract does not state the stimulus concentration or the active range.
    organism
    RAW 264.7 murine macrophages
    plain_language
    (+)-Lariciresinol inhibited reactive oxygen species generation in murine macrophages in a dose-dependent manner without cytotoxicity.
    primary_references
    Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035
    route
    In vitro
    tissue
    Reactive oxygen species generation

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 66–75

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## plus-lariciresinol-lowers-macrophage-ros (+)-Lariciresinol inhibited reactive oxygen species generation in murine macrophages in a dose-dependent manner without cytotoxicity. Model/species: RAW 264.7 murine macrophages Tissue/system: Reactive oxygen species generation Exposure: (+)-Lariciresinol, dose-dependent Route: In vitro Duration: Not stated here Limits: The abstract does not state the stimulus concentration or the active range. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. (+)-Lariciresinol at its minimum inhibitory concentration caused efflux of potassium ions and release of 260 nm absorbing material from Escherichia coli O157:H7 and Staphylococcus aureus, with deteriorated cell wall morphology on electron microscopy.

    (+)-Lariciresinol → Bacterial membrane and cell wall integrity source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Staphylococcus aureus KCTC1621 and Escherichia coli O157:H7
    exposure
    (+)-Lariciresinol at minimum inhibitory concentration; MIC and minimum bactericidal concentration both 125 to 250 µg/mL
    limitations
    The active concentration is roughly 350 to 700 micromolar, two orders of magnitude above the concentrations at which the Nrf2 and enzyme mechanisms operate. Membrane permeabilisation at such concentrations is a low-selectivity mechanism.
    organism
    Staphylococcus aureus KCTC1621 and Escherichia coli O157:H7
    plain_language
    (+)-Lariciresinol at its minimum inhibitory concentration caused efflux of potassium ions and release of 260 nm absorbing material from Escherichia coli O157:H7 and Staphylococcus aureus, with deteriorated cell wall morphology on electron microscopy.
    primary_references
    Efficacy of (+)-Lariciresinol to Control Bacterial Growth of Staphylococcus aureus and Escherichia coli O157:H7. (2017). https://pubmed.ncbi.nlm.nih.gov/28515721/ DOI: 10.3389/fmicb.2017.00804
    route
    In vitro
    tissue
    Bacterial membrane and cell wall integrity

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 231–240

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## plus-lariciresinol-permeabilises-bacterial-membranes (+)-Lariciresinol at its minimum inhibitory concentration caused efflux of potassium ions and release of 260 nm absorbing material from Escherichia coli O157:H7 and Staphylococcus aureus, with deteriorated cell wall morphology on electron microscopy. Model/species: Staphylococcus aureus KCTC1621 and Escherichia coli O157:H7 Tissue/system: Bacterial membrane and cell wall integrity Exposure: (+)-Lariciresinol at minimum inhibitory concentration; MIC and minimum bactericidal concentration both 125 to 250 µg/mL Route: In vitro Duration: Not stated here Limits: The active concentration is roughly 350 to 700 micromolar, two orders of magnitude above the concentrations at which the Nrf2 and enzyme mechanisms operate. Membrane permeabilisation at such concentrations is a low-selectivity mechanism. Primary reference: Efficacy of (+)-Lariciresinol to Control Bacterial Growth of Staphylococcus aureus and Escherichia coli O157:H7. (2017). https://pubmed.ncbi.nlm.nih.gov/28515721/ DOI: 10.3389/fmicb.2017.00804 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  4. (+)-Lariciresinol raised superoxide dismutase, glutathione peroxidase and catalase at transcript and protein level.

    (+)-Lariciresinol → Human copper-zinc superoxide dismutase / SOD1 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    RAW 264.7 murine macrophages
    exposure
    (+)-Lariciresinol
    limitations
    Expression levels, not enzyme activity assays.
    organism
    RAW 264.7 murine macrophages
    plain_language
    (+)-Lariciresinol raised superoxide dismutase, glutathione peroxidase and catalase at transcript and protein level.
    primary_references
    Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035
    route
    In vitro
    tissue
    Antioxidant enzyme expression

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 55–64

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## plus-lariciresinol-raises-antioxidant-enzymes (+)-Lariciresinol raised superoxide dismutase, glutathione peroxidase and catalase at transcript and protein level. Model/species: RAW 264.7 murine macrophages Tissue/system: Antioxidant enzyme expression Exposure: (+)-Lariciresinol Route: In vitro Duration: Not stated here Limits: Expression levels, not enzyme activity assays. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  5. (+)-Lariciresinol increased heme oxygenase 1 at both transcriptional and translational levels, alongside the rise in Nrf2.

    (+)-Lariciresinol → Human heme oxygenase 1 / HMOX1 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    RAW 264.7 murine macrophages
    exposure
    (+)-Lariciresinol
    limitations
    The abstract reports the rise in HO-1 as corresponding to the rise in Nrf2; the causal test by Nrf2 inhibition is described in the full text and was not read here.
    organism
    RAW 264.7 murine macrophages
    plain_language
    (+)-Lariciresinol increased heme oxygenase 1 at both transcriptional and translational levels, alongside the rise in Nrf2.
    primary_references
    Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035
    route
    In vitro
    tissue
    Heme oxygenase 1 expression

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 44–53

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## plus-lariciresinol-raises-heme-oxygenase-1 (+)-Lariciresinol increased heme oxygenase 1 at both transcriptional and translational levels, alongside the rise in Nrf2. Model/species: RAW 264.7 murine macrophages Tissue/system: Heme oxygenase 1 expression Exposure: (+)-Lariciresinol Route: In vitro Duration: Not stated here Limits: The abstract reports the rise in HO-1 as corresponding to the rise in Nrf2; the causal test by Nrf2 inhibition is described in the full text and was not read here. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  6. (+)-Lariciresinol increased Nrf2 at both transcriptional and translational levels.

    (+)-Lariciresinol → Human Nrf2 / NFE2L2 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    RAW 264.7 murine macrophages
    exposure
    (+)-Lariciresinol, dose-dependent, without cytotoxicity
    limitations
    Measured as transcript and protein level rather than as nuclear translocation in the abstract.
    organism
    RAW 264.7 murine macrophages
    plain_language
    (+)-Lariciresinol increased Nrf2 at both transcriptional and translational levels.
    primary_references
    Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035
    route
    In vitro
    tissue
    Nrf2 transcription factor abundance

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 33–42

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## plus-lariciresinol-raises-nrf2 (+)-Lariciresinol increased Nrf2 at both transcriptional and translational levels. Model/species: RAW 264.7 murine macrophages Tissue/system: Nrf2 transcription factor abundance Exposure: (+)-Lariciresinol, dose-dependent, without cytotoxicity Route: In vitro Duration: Not stated here Limits: Measured as transcript and protein level rather than as nuclear translocation in the abstract. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The p38 inhibitor SB239063 suppressed the (+)-lariciresinol-induced response, placing p38 upstream of it.

    p38 mitogen-activated protein kinase family → Human Nrf2 / NFE2L2 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    RAW 264.7 murine macrophages
    exposure
    SB239063 with (+)-lariciresinol
    limitations
    Inhibitor dependence establishes that p38 is required, not that lariciresinol binds or acts on p38 directly.
    organism
    RAW 264.7 murine macrophages
    plain_language
    The p38 inhibitor SB239063 suppressed the (+)-lariciresinol-induced response, placing p38 upstream of it.
    primary_references
    Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035
    route
    In vitro
    tissue
    p38 dependence of the antioxidant response

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 22–31

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## p38-required-for-the-nrf2-response The p38 inhibitor SB239063 suppressed the (+)-lariciresinol-induced response, placing p38 upstream of it. Model/species: RAW 264.7 murine macrophages Tissue/system: p38 dependence of the antioxidant response Exposure: SB239063 with (+)-lariciresinol Route: In vitro Duration: Acute Limits: Inhibitor dependence establishes that p38 is required, not that lariciresinol binds or acts on p38 directly. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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.

    Evidence, AI assistance and curation standards