Component

Lariciresinol, enantiomer unresolved

Aglycone recorded where the report does not state which enantiomer was used.

8 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 inhibited proliferation of hepatoma cells and induced cell cycle arrest in S phase.

    Lariciresinol, enantiomer unresolved → S-phase arrest in HepG2 hepatoma cells 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
    Human HepG2 hepatoma cells
    exposure
    Lariciresinol
    limitations
    No cyclin or cyclin-dependent kinase is identified in the abstract.
    organism
    Human HepG2 hepatoma cells
    plain_language
    Lariciresinol inhibited proliferation of hepatoma cells and induced cell cycle arrest in S phase.
    primary_references
    Proteomic analysis of apoptosis induction by lariciresinol in human HepG2 cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27417256/ DOI: 10.1016/j.cbi.2016.07.013
    route
    In vitro
    tissue
    Cell cycle distribution and proliferation

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 220–229

    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

    ## lariciresinol-arrests-hepatoma-cells-in-s-phase Lariciresinol inhibited proliferation of hepatoma cells and induced cell cycle arrest in S phase. Model/species: Human HepG2 hepatoma cells Tissue/system: Cell cycle distribution and proliferation Exposure: Lariciresinol Route: In vitro Duration: Not stated here Limits: No cyclin or cyclin-dependent kinase is identified in the abstract. Primary reference: Proteomic analysis of apoptosis induction by lariciresinol in human HepG2 cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27417256/ DOI: 10.1016/j.cbi.2016.07.013 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Molecular dynamics simulations indicated lariciresinol was a high-affinity ligand for CXCL10.

    Lariciresinol, enantiomer unresolved → CXCL10 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not applicable
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Molecular docking and molecular dynamics simulation
    exposure
    Lariciresinol, selected among gut microbiota metabolites in a network analysis
    limitations
    A simulated binding result. The study is computational with unspecified in vitro validation and its authors describe it as hypothesis-generating; no cell line, knockdown or binding measurement is reported in the abstract.
    organism
    Molecular docking and molecular dynamics simulation
    plain_language
    Molecular dynamics simulations indicated lariciresinol was a high-affinity ligand for CXCL10.
    primary_references
    Integrative multi-omics analysis identifies CXCL10 as a gut microbiota-associated target in breast cancer. (2025). https://pubmed.ncbi.nlm.nih.gov/41298864/ DOI: 10.1186/s13568-025-01989-0
    route
    In silico
    tissue
    Ligand binding to a chemokine

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 242–251

    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

    ## lariciresinol-binds-cxcl10 Molecular dynamics simulations indicated lariciresinol was a high-affinity ligand for CXCL10. Model/species: Molecular docking and molecular dynamics simulation Tissue/system: Ligand binding to a chemokine Exposure: Lariciresinol, selected among gut microbiota metabolites in a network analysis Route: In silico Duration: Not applicable Limits: A simulated binding result. The study is computational with unspecified in vitro validation and its authors describe it as hypothesis-generating; no cell line, knockdown or binding measurement is reported in the abstract. Primary reference: Integrative multi-omics analysis identifies CXCL10 as a gut microbiota-associated target in breast cancer. (2025). https://pubmed.ncbi.nlm.nih.gov/41298864/ DOI: 10.1186/s13568-025-01989-0 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. Lariciresinol was tested for cellular toxicity and apoptosis induction in fibroblasts, HEK-293 cells and SkBr3 breast cancer cells, alongside podophyllotoxin and pinoresinol.

    Lariciresinol, enantiomer unresolved → Viability of SkBr3, HEK-293 and fibroblast cells source_derived_draftungraded
    Experimental context and source evidence
    duration
    24 and 48 hours
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human fibroblasts, HEK-293 and SkBr3 breast cancer cells
    exposure
    Lariciresinol at a range of concentrations for 24 and 48 hours
    limitations
    The abstract does not give the inhibitory concentrations for each line, so no selectivity between normal and cancer cells can be read from it here. SkBr3 is oestrogen receptor negative, so any activity in this line is independent of that receptor.
    organism
    Human fibroblasts, HEK-293 and SkBr3 breast cancer cells
    plain_language
    Lariciresinol was tested for cellular toxicity and apoptosis induction in fibroblasts, HEK-293 cells and SkBr3 breast cancer cells, alongside podophyllotoxin and pinoresinol.
    primary_references
    The Effect of Podophyllotoxin, Pinoresinol, and Lariciresinol on Cellular Toxicity and Apoptosis Induction in Fibroblast, HEK-293, and SkBr3 Cell Lines. (2024). https://pubmed.ncbi.nlm.nih.gov/38322161/ DOI: 10.30476/IJMS.2023.97113.2939
    route
    In vitro
    tissue
    Cell viability by MTT, apoptosis by flow cytometry, cell cycle and apoptosis regulator gene expression by quantitative PCR

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 253–262

    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

    ## lariciresinol-cytotoxicity-is-not-selective-for-cancer-cells Lariciresinol was tested for cellular toxicity and apoptosis induction in fibroblasts, HEK-293 cells and SkBr3 breast cancer cells, alongside podophyllotoxin and pinoresinol. Model/species: Human fibroblasts, HEK-293 and SkBr3 breast cancer cells Tissue/system: Cell viability by MTT, apoptosis by flow cytometry, cell cycle and apoptosis regulator gene expression by quantitative PCR Exposure: Lariciresinol at a range of concentrations for 24 and 48 hours Route: In vitro Duration: 24 and 48 hours Limits: The abstract does not give the inhibitory concentrations for each line, so no selectivity between normal and cancer cells can be read from it here. SkBr3 is oestrogen receptor negative, so any activity in this line is independent of that receptor. Primary reference: The Effect of Podophyllotoxin, Pinoresinol, and Lariciresinol on Cellular Toxicity and Apoptosis Induction in Fibroblast, HEK-293, and SkBr3 Cell Lines. (2024). https://pubmed.ncbi.nlm.nih.gov/38322161/ DOI: 10.30476/IJMS.2023.97113.2939 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  4. Lariciresinol inhibited α-glucosidase with a half-maximal inhibitory concentration of 6.97 ± 0.37 µM, acting as a competitive inhibitor with an inhibition constant of 0.046 µM.

    Lariciresinol, enantiomer unresolved → Saccharomyces cerevisiae alpha-glucosidase in the 2024 pigment assay source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not applicable
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    α-Glucosidase inhibitory assay with molecular docking
    exposure
    Lariciresinol
    limitations
    The enantiomer is not stated. The inhibition constant is about 150-fold below the inhibitory concentration, which is a large gap for a competitive inhibitor and depends on the substrate concentration used.
    organism
    α-Glucosidase inhibitory assay with molecular docking
    plain_language
    Lariciresinol inhibited α-glucosidase with a half-maximal inhibitory concentration of 6.97 ± 0.37 µM, acting as a competitive inhibitor with an inhibition constant of 0.046 µM.
    primary_references
    Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910
    route
    In vitro
    tissue
    Carbohydrate-hydrolysing enzyme activity

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 165–174

    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

    ## lariciresinol-inhibits-alpha-glucosidase Lariciresinol inhibited α-glucosidase with a half-maximal inhibitory concentration of 6.97 ± 0.37 µM, acting as a competitive inhibitor with an inhibition constant of 0.046 µM. Model/species: α-Glucosidase inhibitory assay with molecular docking Tissue/system: Carbohydrate-hydrolysing enzyme activity Exposure: Lariciresinol Route: In vitro Duration: Not applicable Limits: The enantiomer is not stated. The inhibition constant is about 150-fold below the inhibitory concentration, which is a large gap for a competitive inhibitor and depends on the substrate concentration used. Primary reference: Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  5. Three weeks of oral lariciresinol at 10 mg/kg decreased blood glucose and increased insulin on an oral glucose tolerance test in streptozotocin-treated diabetic mice.

    Lariciresinol, enantiomer unresolved → Blood glucose in streptozotocin-treated diabetic mice source_derived_draftungraded
    Experimental context and source evidence
    duration
    3 weeks
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Streptozotocin-treated diabetic mice
    exposure
    Lariciresinol 10 mg/kg orally for 3 weeks
    limitations
    Streptozotocin-induced diabetes models beta-cell destruction rather than the common human disease, and the enantiomer administered is not stated.
    organism
    Streptozotocin-treated diabetic mice
    plain_language
    Three weeks of oral lariciresinol at 10 mg/kg decreased blood glucose and increased insulin on an oral glucose tolerance test in streptozotocin-treated diabetic mice.
    primary_references
    Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910
    route
    Oral
    tissue
    Blood glucose, insulin and pancreatic histology

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 187–196

    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

    ## lariciresinol-lowers-blood-glucose-in-diabetic-mice Three weeks of oral lariciresinol at 10 mg/kg decreased blood glucose and increased insulin on an oral glucose tolerance test in streptozotocin-treated diabetic mice. Model/species: Streptozotocin-treated diabetic mice Tissue/system: Blood glucose, insulin and pancreatic histology Exposure: Lariciresinol 10 mg/kg orally for 3 weeks Route: Oral Duration: 3 weeks Limits: Streptozotocin-induced diabetes models beta-cell destruction rather than the common human disease, and the enantiomer administered is not stated. Primary reference: Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  6. Lariciresinol lowered heat shock protein 27 in hepatoma cells, confirmed by western blotting, within a set of eight differentially expressed proteins whose network analysis placed the ubiquitin-conjugating enzyme at the hub.

    Lariciresinol, enantiomer unresolved → Heat shock protein 27 / HSPB1 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
    Human HepG2 hepatoma cells
    exposure
    Lariciresinol
    limitations
    Three proteins rose and five fell; the network hub is a computational inference from the eight identified proteins rather than a measured interaction.
    organism
    Human HepG2 hepatoma cells
    plain_language
    Lariciresinol lowered heat shock protein 27 in hepatoma cells, confirmed by western blotting, within a set of eight differentially expressed proteins whose network analysis placed the ubiquitin-conjugating enzyme at the hub.
    primary_references
    Proteomic analysis of apoptosis induction by lariciresinol in human HepG2 cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27417256/ DOI: 10.1016/j.cbi.2016.07.013
    route
    In vitro
    tissue
    Proteome by two-dimensional electrophoresis with western blot confirmation

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 198–207

    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

    ## lariciresinol-lowers-heat-shock-protein-27 Lariciresinol lowered heat shock protein 27 in hepatoma cells, confirmed by western blotting, within a set of eight differentially expressed proteins whose network analysis placed the ubiquitin-conjugating enzyme at the hub. Model/species: Human HepG2 hepatoma cells Tissue/system: Proteome by two-dimensional electrophoresis with western blot confirmation Exposure: Lariciresinol Route: In vitro Duration: Not stated here Limits: Three proteins rose and five fell; the network hub is a computational inference from the eight identified proteins rather than a measured interaction. Primary reference: Proteomic analysis of apoptosis induction by lariciresinol in human HepG2 cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27417256/ DOI: 10.1016/j.cbi.2016.07.013 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  7. Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot.

    Lariciresinol, enantiomer unresolved → Inner mitochondrial membrane potential 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
    Human HepG2 hepatoma cells
    exposure
    Lariciresinol, dose-dependent
    limitations
    The enantiomer is not stated, and the abstract does not give the concentration range or the inhibitory concentration.
    organism
    Human HepG2 hepatoma cells
    plain_language
    Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot.
    primary_references
    Lariciresinol induces apoptosis in HepG2 cells via mitochondrial-mediated apoptosis pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29247613/ DOI: 10.1016/j.ejphar.2017.12.015
    route
    In vitro
    tissue
    Mitochondrial membrane potential and apoptosis-associated proteins

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 209–218

    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

    ## lariciresinol-lowers-mitochondrial-membrane-potential Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot. Model/species: Human HepG2 hepatoma cells Tissue/system: Mitochondrial membrane potential and apoptosis-associated proteins Exposure: Lariciresinol, dose-dependent Route: In vitro Duration: Not stated here Limits: The enantiomer is not stated, and the abstract does not give the concentration range or the inhibitory concentration. Primary reference: Lariciresinol induces apoptosis in HepG2 cells via mitochondrial-mediated apoptosis pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29247613/ DOI: 10.1016/j.ejphar.2017.12.015 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  8. In C2C12 myotubes lariciresinol activated insulin signalling leading to GLUT4 translocation and augmented glucose uptake.

    Lariciresinol, enantiomer unresolved → GLUT4 translocation in C2C12 myotubes 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
    C2C12 myotubes
    exposure
    Lariciresinol
    limitations
    The enantiomer and the concentrations are not stated in the abstract. The abstract describes insulin signalling and GSK-3β and does not report AMPK.
    organism
    C2C12 myotubes
    plain_language
    In C2C12 myotubes lariciresinol activated insulin signalling leading to GLUT4 translocation and augmented glucose uptake.
    primary_references
    Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910
    route
    In vitro
    tissue
    Insulin signalling and glucose transporter translocation

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 176–185

    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

    ## lariciresinol-moves-glut4-and-raises-glucose-uptake In C2C12 myotubes lariciresinol activated insulin signalling leading to GLUT4 translocation and augmented glucose uptake. Model/species: C2C12 myotubes Tissue/system: Insulin signalling and glucose transporter translocation Exposure: Lariciresinol Route: In vitro Duration: Not stated here Limits: The enantiomer and the concentrations are not stated in the abstract. The abstract describes insulin signalling and GSK-3β and does not report AMPK. Primary reference: Lariciresinol Displays Anti-Diabetic Activity through Inhibition of α-Glucosidase and Activation and Enhancement of Insulin Signaling. (2022). https://pubmed.ncbi.nlm.nih.gov/35490401/ DOI: 10.1002/mnfr.202100910 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