Apigenin 7-O-glucuronide

evidence_access

Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.

experimental_condition

LPS alone Apigenin 7-O-glucuronide plus LPS · Apigenin 7-O-glucuronide Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_condition

LPS alone LPS challenge · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "Apigenin 7-O-glucuronide plus LPS", "comparator": "LPS alone", "endpoint": "Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin-7-glucuronide", "state": "Apigenin 7-O-glucuronide plus LPS"}, {"entity_slug": "lipopolysaccharide", "state": "LPS challenge"}]} Explicit extracted experimental comparison; recorded from source.

experimental_model

Mouse macrophage cell line; exposure details unavailable in the accessed abstract.

interpretation_status

Recorded from source with stated access limits; ungraded, not independent replication.

limitations

Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.

nutrient_topic

Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin

plain_language

Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells.

primary_references

Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k

source_locator

Reviewed reference api-glucuronide-activity; Do not assume conjugates are inert or assume intracellular parent regeneration; intracellular speciation was not established by this abstract.

Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 130–136

AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse macrophage cell line; exposure details unavailable in the accessed abstract. · Recorded from source · Recorded from source

### api-glucuronide-activity Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells. Do not assume conjugates are inert or assume intracellular parent regeneration; intracellular speciation was not established by this abstract. Model and exposure: Mouse macrophage cell line; exposure details unavailable in the accessed abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | 2016 | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.

evidence_access

Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.

experimental_condition

LPS alone Glucuronide plus LPS · Apigenin 7-O-glucuronide Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_condition

LPS alone LPS challenge · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "Glucuronide plus LPS", "comparator": "LPS alone", "endpoint": "The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin-7-glucuronide", "state": "Glucuronide plus LPS"}, {"entity_slug": "lipopolysaccharide", "state": "LPS challenge"}]} Explicit extracted experimental comparison; recorded from source.

experimental_model

LPS-stimulated mouse RAW264.7 cells; primary abstract.

interpretation_status

Recorded from source with stated access limits; ungraded, not independent replication.

limitations

Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.

nutrient_topic

Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin

plain_language

The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model.

primary_references

Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k

source_locator

Reviewed reference api-glucuronide-ap1; Signaling and expression observations are not direct binding measurements.

Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 138–144

AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · LPS-stimulated mouse RAW264.7 cells; primary abstract. · Recorded from source · Recorded from source

### api-glucuronide-ap1 The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model. Signaling and expression observations are not direct binding measurements. Model and exposure: LPS-stimulated mouse RAW264.7 cells; primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | 2016 | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.

evidence_access

Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.

experimental_contrast

{"intervention": "Glucuronide concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.

experimental_model

Table 1; ATP 20 micromolar; isolated catalytic subunit, not holoenzyme.

interpretation_status

Recorded from source with stated access limits; ungraded, not independent replication.

limitations

Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.

nutrient_topic

Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin

plain_language

Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate.

primary_references

Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1

source_locator

Reviewed reference api-glucuronide-ck2; A conjugate can retain assay activity; this does not establish its cellular uptake or direct in-vivo effect.

Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 632–638

AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Table 1; ATP 20 micromolar; isolated catalytic subunit, not holoenzyme. · Recorded from source · Recorded from source

### api-glucuronide-ck2 Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate. A conjugate can retain assay activity; this does not establish its cellular uptake or direct in-vivo effect. Model and exposure: Table 1; ATP 20 micromolar; isolated catalytic subunit, not holoenzyme. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.

evidence_access

Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.

experimental_model

Three healthy men; authentic-standard HPLC-MS.

interpretation_status

Recorded from source with stated access limits; ungraded, not independent replication.

limitations

Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.

nutrient_topic

Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin

plain_language

The same aglycone exposure yielded 0.9 ± 0.6 micromoles of measured urinary glucuronides over 24 hours, about 0.5% of intake.

primary_references

Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007

source_locator

Reviewed reference api-parent-urine; Recovery of selected metabolites is not an absolute bioavailability measurement.

Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 37–43

AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Three healthy men; authentic-standard HPLC-MS. · Recorded from source · Recorded from source

### api-parent-urine The same aglycone exposure yielded 0.9 ± 0.6 micromoles of measured urinary glucuronides over 24 hours, about 0.5% of intake. Recovery of selected metabolites is not an absolute bioavailability measurement. Model and exposure: Three healthy men; authentic-standard HPLC-MS. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.

evidence_access

Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.

experimental_model

Four men; 0–24-hour urine.

interpretation_status

Recorded from source with stated access limits; ungraded, not independent replication.

limitations

Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.

nutrient_topic

Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin

plain_language

Measured urinary apigenin metabolites after the initial parsley drink averaged 11.2% of ingested flavone equivalents.

primary_references

Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007

source_locator

Reviewed reference api-parsley-urine; The larger repeated-intake series gave 17.2 ± 9.8% recovery across 17 intakes, with greater inter-person than within-person variation. Neither figure is an intravenous-reference absolute bioavailability estimate.

Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 61–67

AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Four men; 0–24-hour urine. · Recorded from source · Recorded from source

### api-parsley-urine Measured urinary apigenin metabolites after the initial parsley drink averaged 11.2% of ingested flavone equivalents. The larger repeated-intake series gave 17.2 ± 9.8% recovery across 17 intakes, with greater inter-person than within-person variation. Neither figure is an intravenous-reference absolute bioavailability estimate. Model and exposure: Four men; 0–24-hour urine. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.