Naringenin

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.