Component
Mouse hepatic NLRP3/NF-kappaB inflammation
Species, preparation, dose and limitations are retained on linked claims.
1 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Naringenin reduced lipid accumulation and inflammatory signaling in methionine/choline-deficient mice and cells; effects were lost in NLRP3-null hepatocytes and restored after NLRP3 re-expression.
Experimental context and source evidence
- dose
- Naringenin 100 mg/kg/day by gavage in the mouse arm
- duration
- 7 days in mice
- 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
- Wild-type and NLRP3-knockout mice; HepG2 cells, hepatocytes and Kupffer cells
- limitations
- The methionine/choline-deficient model and high dose do not reproduce ordinary citrus intake or all human NAFLD.
- nutrient_topic
- Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
- organism
- Wild-type and NLRP3-knockout mice; HepG2 cells, hepatocytes and Kupffer cells
- plain_language
- Naringenin reduced lipid accumulation and inflammatory signaling in methionine/choline-deficient mice and cells; effects were lost in NLRP3-null hepatocytes and restored after NLRP3 re-expression.
- primary_references
- Naringenin attenuates non-alcoholic fatty liver disease by down-regulating the NLRP3/NF-κB pathway in mice. (2020). https://pubmed.ncbi.nlm.nih.gov/31758699/ DOI: 10.1111/bph.14938
- route
- Oral and in vitro
- tissue
- NAFLD lipid accumulation and NLRP3/NF-kappaB signaling
Naringenin: mechanism of action and interactions (2026-09-20) · lines 121–130
Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Wild-type and NLRP3-knockout mice; HepG2 cells, hepatocytes and Kupffer cells · source_derived_draft · unverified_draft
## naringenin-nlrp3-dependence Naringenin reduced lipid accumulation and inflammatory signaling in methionine/choline-deficient mice and cells; effects were lost in NLRP3-null hepatocytes and restored after NLRP3 re-expression. Model/species: Wild-type and NLRP3-knockout mice; HepG2 cells, hepatocytes and Kupffer cells Tissue/system: NAFLD lipid accumulation and NLRP3/NF-kappaB signaling Exposure: Naringenin 100 mg/kg/day by gavage in the mouse arm Route: Oral and in vitro Duration: 7 days in mice Limits: The methionine/choline-deficient model and high dose do not reproduce ordinary citrus intake or all human NAFLD. Primary reference: Naringenin attenuates non-alcoholic fatty liver disease by down-regulating the NLRP3/NF-κB pathway in mice. (2020). https://pubmed.ncbi.nlm.nih.gov/31758699/ DOI: 10.1111/bph.14938 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.