Component

Hericenone E

Species, preparation, dose and limitations are retained on linked claims.

2 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.

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

Where it participates (unsigned role)

  1. Purified hericenones C, D and E failed to promote NGF gene expression in the 1321N1 assay that responded to the whole extract.

    Experimental context and source evidence
    dose
    Purified hericenones C, D and E
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human 1321N1 astrocytoma cells
    limitations
    This source-specific null prevents assigning the extract's NGF induction to those three molecules; other assays may differ.
    nutrient_topic
    Hericenones & Erinacines chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Hericenones and erinacines
    organism
    Human 1321N1 astrocytoma cells
    plain_language
    Purified hericenones C, D and E failed to promote NGF gene expression in the 1321N1 assay that responded to the whole extract.
    primary_references
    Nerve growth factor-inducing activity of Hericium erinaceus in 1321N1 human astrocytoma cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18758067/ DOI: 10.1248/bpb.31.1727
    route
    In vitro
    tissue
    NGF gene expression

    Hericenones & Erinacines: mechanism of action and interactions (2026-09-20) · lines 22–31

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Human 1321N1 astrocytoma cells · source_derived_draft · unverified_draft

    ## hericenones-erinacines-hericenone-cde-null Purified hericenones C, D and E failed to promote NGF gene expression in the 1321N1 assay that responded to the whole extract. Model/species: Human 1321N1 astrocytoma cells Tissue/system: NGF gene expression Exposure: Purified hericenones C, D and E Route: In vitro Duration: Acute Limits: This source-specific null prevents assigning the extract's NGF induction to those three molecules; other assays may differ. Primary reference: Nerve growth factor-inducing activity of Hericium erinaceus in 1321N1 human astrocytoma cells. (2008). https://pubmed.ncbi.nlm.nih.gov/18758067/ DOI: 10.1248/bpb.31.1727 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence
  2. K252a partially blocked hericenone-E-associated neuritogenesis, while hericenone E increased NGF secretion and ERK/Akt phosphorylation.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Hericenone E with low NGF and K252a
    duration
    Differentiation assay
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Rat PC12 pheochromocytoma cells
    limitations
    Partial blockade suggests Trk involvement but not sole dependence; PC12 exposure does not establish human brain target engagement.
    nutrient_topic
    Hericenones & Erinacines chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Hericenones and erinacines
    organism
    Rat PC12 pheochromocytoma cells
    plain_language
    K252a partially blocked hericenone-E-associated neuritogenesis, while hericenone E increased NGF secretion and ERK/Akt phosphorylation.
    primary_references
    Hericium erinaceus (Bull.: Fr) Pers. cultivated under tropical conditions: isolation of hericenones and demonstration of NGF-mediated neurite outgrowth in PC12 cells via MEK/ERK and PI3K-Akt signaling pathways. (2014). https://pubmed.ncbi.nlm.nih.gov/25288148/ DOI: 10.1039/c4fo00452c
    route
    In vitro
    tissue
    NGF secretion, neurite outgrowth, ERK and Akt
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Hericenones & Erinacines: mechanism of action and interactions (2026-09-20) · lines 44–53

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Rat PC12 pheochromocytoma cells · source_derived_draft · unverified_draft

    ## hericenones-erinacines-hericenone-e-ngf K252a partially blocked hericenone-E-associated neuritogenesis, while hericenone E increased NGF secretion and ERK/Akt phosphorylation. Model/species: Rat PC12 pheochromocytoma cells Tissue/system: NGF secretion, neurite outgrowth, ERK and Akt Exposure: Hericenone E with low NGF and K252a Route: In vitro Duration: Differentiation assay Limits: Partial blockade suggests Trk involvement but not sole dependence; PC12 exposure does not establish human brain target engagement. Primary reference: Hericium erinaceus (Bull.: Fr) Pers. cultivated under tropical conditions: isolation of hericenones and demonstration of NGF-mediated neurite outgrowth in PC12 cells via MEK/ERK and PI3K-Akt signaling pathways. (2014). https://pubmed.ncbi.nlm.nih.gov/25288148/ DOI: 10.1039/c4fo00452c 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