Nutrient chapter

Naringenin

A citrus flavanone aglycone. Naringin is a separate glycoside precursor; circulating sulfate and glucuronide conjugates are separate chemical species.

13 recorded mechanisms · 1 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

  1. Whole-orange extract supplying 150-900 mg naringenin produced dose-related serum exposure in 18 adults; half-life was about 2.65-3.0 hours at the fully profiled doses.

    Naringenin → Human serum naringenin after conjugate hydrolysis source_derived_draftungraded
    Experimental context and source evidence
    dose
    150, 300, 600 or 900 mg naringenin in whole-orange extract
    duration
    24 hours with at least one-week washout
    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
    Eighteen healthy adults in a randomized crossover trial
    limitations
    The assay reported total released aglycone after hydrolysis and does not equal free circulating naringenin; this was a single-dose safety/PK trial.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Eighteen healthy adults in a randomized crossover trial
    plain_language
    Whole-orange extract supplying 150-900 mg naringenin produced dose-related serum exposure in 18 adults; half-life was about 2.65-3.0 hours at the fully profiled doses.
    primary_references
    Safety and pharmacokinetics of naringenin: A randomized, controlled, single-ascending-dose clinical trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31468636/ DOI: 10.1111/dom.13868
    route
    Oral
    tissue
    Serum LC-MS after beta-glucuronidase/sulfatase hydrolysis

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 11–20

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Eighteen healthy adults in a randomized crossover trial · source_derived_draft · unverified_draft

    ## naringenin-human-pk Whole-orange extract supplying 150-900 mg naringenin produced dose-related serum exposure in 18 adults; half-life was about 2.65-3.0 hours at the fully profiled doses. Model/species: Eighteen healthy adults in a randomized crossover trial Tissue/system: Serum LC-MS after beta-glucuronidase/sulfatase hydrolysis Exposure: 150, 300, 600 or 900 mg naringenin in whole-orange extract Route: Oral Duration: 24 hours with at least one-week washout Limits: The assay reported total released aglycone after hydrolysis and does not equal free circulating naringenin; this was a single-dose safety/PK trial. Primary reference: Safety and pharmacokinetics of naringenin: A randomized, controlled, single-ascending-dose clinical trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31468636/ DOI: 10.1111/dom.13868 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Human fecal-water preparations converted naringin to naringenin in vitro.

    Naringin → Naringenin source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringin incubation
    duration
    Sampling through the incubation
    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
    Fecal water from six human donors
    limitations
    Fecal-water conversion does not quantify in-vivo absorption or identify all organisms and enzymes.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Fecal water from six human donors
    plain_language
    Human fecal-water preparations converted naringin to naringenin in vitro.
    primary_references
    Human intestinal microbial metabolism of naringin. (2015). https://pubmed.ncbi.nlm.nih.gov/24935725/ DOI: 10.1007/s13318-014-0193-x
    route
    Ex vivo human microbial incubation
    tissue
    Anaerobic intestinal-microbial metabolism

    Naringenin: 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 · Fecal water from six human donors · source_derived_draft · unverified_draft

    ## naringenin-naringin-conversion Human fecal-water preparations converted naringin to naringenin in vitro. Model/species: Fecal water from six human donors Tissue/system: Anaerobic intestinal-microbial metabolism Exposure: Naringin incubation Route: Ex vivo human microbial incubation Duration: Sampling through the incubation Limits: Fecal-water conversion does not quantify in-vivo absorption or identify all organisms and enzymes. Primary reference: Human intestinal microbial metabolism of naringin. (2015). https://pubmed.ncbi.nlm.nih.gov/24935725/ DOI: 10.1007/s13318-014-0193-x Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. One donor's fecal water produced 4-HPPA from naringenin, while downstream 4-HPPA degradation differed among 22 donors.

    Naringenin → 3-(4-Hydroxyphenyl)propionic acid / 4-HPPA source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin or 4-HPPA incubation
    duration
    Incubation study
    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 fecal incubations from six and then 22 donors
    limitations
    Absence of measured 4-HPPA in five donors may reflect faster downstream degradation rather than absent formation.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Human fecal incubations from six and then 22 donors
    plain_language
    One donor's fecal water produced 4-HPPA from naringenin, while downstream 4-HPPA degradation differed among 22 donors.
    primary_references
    Human intestinal microbial metabolism of naringin. (2015). https://pubmed.ncbi.nlm.nih.gov/24935725/ DOI: 10.1007/s13318-014-0193-x
    route
    Ex vivo
    tissue
    Microbial naringenin and 4-HPPA metabolism

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 33–42

    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 fecal incubations from six and then 22 donors · source_derived_draft · unverified_draft

    ## naringenin-microbial-hppa One donor's fecal water produced 4-HPPA from naringenin, while downstream 4-HPPA degradation differed among 22 donors. Model/species: Human fecal incubations from six and then 22 donors Tissue/system: Microbial naringenin and 4-HPPA metabolism Exposure: Naringenin or 4-HPPA incubation Route: Ex vivo Duration: Incubation study Limits: Absence of measured 4-HPPA in five donors may reflect faster downstream degradation rather than absent formation. Primary reference: Human intestinal microbial metabolism of naringin. (2015). https://pubmed.ncbi.nlm.nih.gov/24935725/ DOI: 10.1007/s13318-014-0193-x Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  4. Perfused mouse intestine absorbed naringenin well but returned mostly sulfate and then glucuronide metabolites to the lumen, indicating extensive intestinal first-pass metabolism.

    Naringenin → Mouse intestinal first-pass sulfate and glucuronide conjugation source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin 3.5 micrograms/mL
    duration
    60 minutes
    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
    Single-pass stomach, small-intestine and colon perfusion in mice
    limitations
    Mouse permeability and metabolite fractions do not define human oral bioavailability.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Single-pass stomach, small-intestine and colon perfusion in mice
    plain_language
    Perfused mouse intestine absorbed naringenin well but returned mostly sulfate and then glucuronide metabolites to the lumen, indicating extensive intestinal first-pass metabolism.
    primary_references
    High gastrointestinal permeability and local metabolism of naringenin: influence of antibiotic treatment on absorption and metabolism. (2015). https://pubmed.ncbi.nlm.nih.gov/26083965/ DOI: 10.1017/S0007114515001671
    route
    In-situ intestinal perfusion
    tissue
    Permeability and phase-II metabolites

    Naringenin: 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 · Single-pass stomach, small-intestine and colon perfusion in mice · source_derived_draft · unverified_draft

    ## naringenin-intestinal-first-pass Perfused mouse intestine absorbed naringenin well but returned mostly sulfate and then glucuronide metabolites to the lumen, indicating extensive intestinal first-pass metabolism. Model/species: Single-pass stomach, small-intestine and colon perfusion in mice Tissue/system: Permeability and phase-II metabolites Exposure: Naringenin 3.5 micrograms/mL Route: In-situ intestinal perfusion Duration: 60 minutes Limits: Mouse permeability and metabolite fractions do not define human oral bioavailability. Primary reference: High gastrointestinal permeability and local metabolism of naringenin: influence of antibiotic treatment on absorption and metabolism. (2015). https://pubmed.ncbi.nlm.nih.gov/26083965/ DOI: 10.1017/S0007114515001671 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  5. Five days of rifaximin reduced colonic naringenin permeability and lowered luminal 4-hydroxyhippuric and hippuric acids in mice.

    Rifaximin → Mouse colonic naringenin permeability source_derived_draftungraded
    Experimental context and source evidence
    dose
    Rifaximin 50 mg/kg/day for 5 days; naringenin 3.5 micrograms/mL
    duration
    5 days plus 60-minute perfusion
    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
    Mice undergoing colonic perfusion
    limitations
    The antibiotic changes multiple microbial and host processes; this does not support using rifaximin to control naringenin exposure.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Mice undergoing colonic perfusion
    plain_language
    Five days of rifaximin reduced colonic naringenin permeability and lowered luminal 4-hydroxyhippuric and hippuric acids in mice.
    primary_references
    High gastrointestinal permeability and local metabolism of naringenin: influence of antibiotic treatment on absorption and metabolism. (2015). https://pubmed.ncbi.nlm.nih.gov/26083965/ DOI: 10.1017/S0007114515001671
    route
    Oral pretreatment and in-situ perfusion
    tissue
    Antibiotic perturbation of absorption and microbial products

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 55–64

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Mice undergoing colonic perfusion · source_derived_draft · unverified_draft

    ## naringenin-rifaximin-effect Five days of rifaximin reduced colonic naringenin permeability and lowered luminal 4-hydroxyhippuric and hippuric acids in mice. Model/species: Mice undergoing colonic perfusion Tissue/system: Antibiotic perturbation of absorption and microbial products Exposure: Rifaximin 50 mg/kg/day for 5 days; naringenin 3.5 micrograms/mL Route: Oral pretreatment and in-situ perfusion Duration: 5 days plus 60-minute perfusion Limits: The antibiotic changes multiple microbial and host processes; this does not support using rifaximin to control naringenin exposure. Primary reference: High gastrointestinal permeability and local metabolism of naringenin: influence of antibiotic treatment on absorption and metabolism. (2015). https://pubmed.ncbi.nlm.nih.gov/26083965/ DOI: 10.1017/S0007114515001671 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  6. Naringenin sulfate conjugates formed more stable complexes with human serum albumin than the parent flavonoid in vitro.

    Naringenin sulfate conjugates → Human serum albumin source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin and sulfate/glucuronide conjugates
    duration
    Equilibrium 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
    Cell-free human serum albumin binding assays
    limitations
    Binding does not establish tissue delivery or a clinically important displacement interaction.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Cell-free human serum albumin binding assays
    plain_language
    Naringenin sulfate conjugates formed more stable complexes with human serum albumin than the parent flavonoid in vitro.
    primary_references
    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078
    route
    In vitro
    tissue
    Ligand-protein binding

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 66–75

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Cell-free human serum albumin binding assays · source_derived_draft · unverified_draft

    ## naringenin-conjugate-albumin Naringenin sulfate conjugates formed more stable complexes with human serum albumin than the parent flavonoid in vitro. Model/species: Cell-free human serum albumin binding assays Tissue/system: Ligand-protein binding Exposure: Naringenin and sulfate/glucuronide conjugates Route: In vitro Duration: Equilibrium assay Limits: Binding does not establish tissue delivery or a clinically important displacement interaction. Primary reference: Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  7. Naringenin sulfate and glucuronide conjugates showed no or only weak inhibition of CYP2C9, CYP2C19 and CYP3A4 in the tested assays.

    Naringenin sulfate conjugates → Human CYP2C9/CYP2C19/CYP3A4 assay panel source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin conjugate concentration series
    duration
    Acute enzyme incubation
    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 CYP enzyme assays
    limitations
    This is a useful negative/weak result for the tested enzymes, not a complete drug-interaction screen.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Human CYP enzyme assays
    plain_language
    Naringenin sulfate and glucuronide conjugates showed no or only weak inhibition of CYP2C9, CYP2C19 and CYP3A4 in the tested assays.
    primary_references
    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078
    route
    In vitro
    tissue
    CYP2C9, CYP2C19 and CYP3A4 activity

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 77–86

    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 CYP enzyme assays · source_derived_draft · unverified_draft

    ## naringenin-cyp-weak-null Naringenin sulfate and glucuronide conjugates showed no or only weak inhibition of CYP2C9, CYP2C19 and CYP3A4 in the tested assays. Model/species: Human CYP enzyme assays Tissue/system: CYP2C9, CYP2C19 and CYP3A4 activity Exposure: Naringenin conjugate concentration series Route: In vitro Duration: Acute enzyme incubation Limits: This is a useful negative/weak result for the tested enzymes, not a complete drug-interaction screen. Primary reference: Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  8. Selected naringenin sulfate or glucuronide conjugates potently inhibited OATP1B1 and/or OATP2B1 in vitro.

    Naringenin sulfate conjugates → Human OATP1B1/OATP2B1 transport activity source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin metabolite concentration-response
    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
    Transporter expression assays
    limitations
    The abstract does not assign every conjugate to each transporter or establish interaction at human free concentrations.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Transporter expression assays
    plain_language
    Selected naringenin sulfate or glucuronide conjugates potently inhibited OATP1B1 and/or OATP2B1 in vitro.
    primary_references
    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078
    route
    In vitro
    tissue
    OATP1B1 and OATP2B1 transport

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 88–97

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

    ## naringenin-oatp-inhibition Selected naringenin sulfate or glucuronide conjugates potently inhibited OATP1B1 and/or OATP2B1 in vitro. Model/species: Transporter expression assays Tissue/system: OATP1B1 and OATP2B1 transport Exposure: Naringenin metabolite concentration-response Route: In vitro Duration: Acute Limits: The abstract does not assign every conjugate to each transporter or establish interaction at human free concentrations. Primary reference: Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  9. Naringenin and its sulfate/glucuronide metabolites were weak inhibitors of xanthine oxidase in xanthine and 6-mercaptopurine oxidation assays.

    Naringenin → Xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin, sulfate and glucuronide conjugates
    duration
    Acute enzyme incubation
    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
    Cell-free xanthine oxidase assays
    limitations
    Luteolin and myricetin species were the potent inhibitors in this study; the weak naringenin result does not establish a clinical 6-mercaptopurine interaction.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Cell-free xanthine oxidase assays
    plain_language
    Naringenin and its sulfate/glucuronide metabolites were weak inhibitors of xanthine oxidase in xanthine and 6-mercaptopurine oxidation assays.
    primary_references
    Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. (2023). https://pubmed.ncbi.nlm.nih.gov/37734263/ DOI: 10.1016/j.biopha.2023.115548
    route
    In vitro
    tissue
    Xanthine and 6-mercaptopurine oxidation

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 99–108

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Cell-free xanthine oxidase assays · source_derived_draft · unverified_draft

    ## naringenin-xo-weak Naringenin and its sulfate/glucuronide metabolites were weak inhibitors of xanthine oxidase in xanthine and 6-mercaptopurine oxidation assays. Model/species: Cell-free xanthine oxidase assays Tissue/system: Xanthine and 6-mercaptopurine oxidation Exposure: Naringenin, sulfate and glucuronide conjugates Route: In vitro Duration: Acute enzyme incubation Limits: Luteolin and myricetin species were the potent inhibitors in this study; the weak naringenin result does not establish a clinical 6-mercaptopurine interaction. Primary reference: Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. (2023). https://pubmed.ncbi.nlm.nih.gov/37734263/ DOI: 10.1016/j.biopha.2023.115548 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  10. Naringenin severely inhibited Enterococcus caccae, slightly enhanced Bifidobacterium catenulatum, and did not change Ruminococcus gauvreauii growth in culture.

    Naringenin → Growth of selected human gut commensals source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin exposure
    duration
    Time-course culture
    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
    Three cultured human commensal bacterial species
    limitations
    Three isolated species do not represent community-level or in-vivo microbiome effects.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Three cultured human commensal bacterial species
    plain_language
    Naringenin severely inhibited Enterococcus caccae, slightly enhanced Bifidobacterium catenulatum, and did not change Ruminococcus gauvreauii growth in culture.
    primary_references
    Analysis of Temporal Changes in Growth and Gene Expression for Commensal Gut Microbes in Response to the Polyphenol Naringenin. (2018). https://pubmed.ncbi.nlm.nih.gov/30013359/ DOI: 10.1177/1178636118775100
    route
    In vitro microbial culture
    tissue
    Growth curves and single-molecule RNA sequencing

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 110–119

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Three cultured human commensal bacterial species · source_derived_draft · unverified_draft

    ## naringenin-microbial-growth-selectivity Naringenin severely inhibited Enterococcus caccae, slightly enhanced Bifidobacterium catenulatum, and did not change Ruminococcus gauvreauii growth in culture. Model/species: Three cultured human commensal bacterial species Tissue/system: Growth curves and single-molecule RNA sequencing Exposure: Naringenin exposure Route: In vitro microbial culture Duration: Time-course culture Limits: Three isolated species do not represent community-level or in-vivo microbiome effects. Primary reference: Analysis of Temporal Changes in Growth and Gene Expression for Commensal Gut Microbes in Response to the Polyphenol Naringenin. (2018). https://pubmed.ncbi.nlm.nih.gov/30013359/ DOI: 10.1177/1178636118775100 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  11. 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.

    Naringenin → Mouse hepatic NLRP3/NF-kappaB inflammation source_derived_draftungraded
    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

  12. AMPK inhibition reversed naringenin-induced autophagy in LPS-stimulated macrophages, while Atg5 silencing or chloroquine counteracted its cytokine effect.

    Experimental AMPK inhibition → Naringenin-induced macrophage autophagy source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Naringenin with AMPK inhibition, Atg5 silencing or chloroquine
    duration
    Acute cell 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
    LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm
    limitations
    The inhibitor and silencing experiments support pathway dependence in this model, not rheumatoid-arthritis efficacy in humans.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm
    plain_language
    AMPK inhibition reversed naringenin-induced autophagy in LPS-stimulated macrophages, while Atg5 silencing or chloroquine counteracted its cytokine effect.
    primary_references
    Naringenin ameliorates collagen-induced arthritis through activating AMPK-mediated autophagy in macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37904715/ DOI: 10.1002/iid3.983
    route
    In vitro perturbation
    tissue
    AMPK/ULK1 autophagic flux and cytokines
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 132–141

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm · source_derived_draft · unverified_draft

    ## naringenin-ampk-autophagy-dependence AMPK inhibition reversed naringenin-induced autophagy in LPS-stimulated macrophages, while Atg5 silencing or chloroquine counteracted its cytokine effect. Model/species: LPS-stimulated RAW264.7 macrophages with a collagen-induced-arthritis mouse arm Tissue/system: AMPK/ULK1 autophagic flux and cytokines Exposure: Naringenin with AMPK inhibition, Atg5 silencing or chloroquine Route: In vitro perturbation Duration: Acute cell assay Limits: The inhibitor and silencing experiments support pathway dependence in this model, not rheumatoid-arthritis efficacy in humans. Primary reference: Naringenin ameliorates collagen-induced arthritis through activating AMPK-mediated autophagy in macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37904715/ DOI: 10.1002/iid3.983 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  13. SIRT1 siRNA diminished naringenin-associated improvements in endothelial senescence, oxidative stress and mitochondrial injury.

    Experimental SIRT1 siRNA suppression → Naringenin response in oxidatively stressed endothelial cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin with SIRT1 siRNA
    duration
    Cell experiment accompanying three-month mouse dosing
    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
    Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm
    limitations
    SIRT1 involvement in a cell model does not establish direct SIRT1 binding or human atherosclerosis treatment.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm
    plain_language
    SIRT1 siRNA diminished naringenin-associated improvements in endothelial senescence, oxidative stress and mitochondrial injury.
    primary_references
    Naringenin ameliorates vascular senescence and atherosclerosis involving SIRT1 activation. (2023). https://pubmed.ncbi.nlm.nih.gov/37343148/ DOI: 10.1093/jpp/rgad053
    route
    In vitro perturbation
    tissue
    SIRT1, FOXO3a/PGC1alpha and senescence measures

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 143–152

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm · source_derived_draft · unverified_draft

    ## naringenin-sirt1-silencing SIRT1 siRNA diminished naringenin-associated improvements in endothelial senescence, oxidative stress and mitochondrial injury. Model/species: Hydrogen-peroxide-stressed endothelial cells; aged ApoE-null mouse arm Tissue/system: SIRT1, FOXO3a/PGC1alpha and senescence measures Exposure: Naringenin with SIRT1 siRNA Route: In vitro perturbation Duration: Cell experiment accompanying three-month mouse dosing Limits: SIRT1 involvement in a cell model does not establish direct SIRT1 binding or human atherosclerosis treatment. Primary reference: Naringenin ameliorates vascular senescence and atherosclerosis involving SIRT1 activation. (2023). https://pubmed.ncbi.nlm.nih.gov/37343148/ DOI: 10.1093/jpp/rgad053 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

AMPK or autophagy disruption counteracts the macrophage response to naringenin

Condition: machinery_impairment · AMPK is inhibited, Atg5 is silenced, or autophagolysosome function is blocked by chloroquine.

Normal role: Naringenin activates AMPK/ULK1 and autophagic flux in the model.

Recorded consequence: Autophagy initiation or the cytokine effect is counteracted.

Scope: In-vitro macrophage perturbation.

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

  • Naringenin: mechanism of action and interactions (2026-09-20)Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

    Open questions in this collection

    Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

      Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

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      Evidence, AI assistance and curation standards