Human caspase-3 / CASP3

dose

Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract

duration

3 h

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Human isolated red blood cells challenged with cigarette smoke extract

limitations

An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Human isolated red blood cells challenged with cigarette smoke extract

plain_language

Indicaxanthin reduced smoke-extract-induced caspase-3 cleavage and activity in red cells.

primary_references

Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051

route

Ex vivo co-incubation

tissue

Erythrocyte membrane and cytosol

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 467–475

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human isolated red blood cells challenged with cigarette smoke extract · source_derived_draft · unverified_draft

## betalains-redcell-casp3 Indicaxanthin reduced smoke-extract-induced caspase-3 cleavage and activity in red cells. Model/species: Human isolated red blood cells challenged with cigarette smoke extract Tissue: Erythrocyte membrane and cytosol Exposure: Indicaxanthin 1-5 micromolar; aqueous cigarette smoke extract Route: Ex vivo co-incubation Duration: 3 h Limits: An isolated-cell smoke-extract experiment does not establish protection against smoking-related disease; no direct Fas-binding assay was reported in the abstract. Primary reference: Indicaxanthin prevents eryptosis induced by cigarette smoke extract by interfering with active Fas-mediated signaling. (2024). https://pubmed.ncbi.nlm.nih.gov/38520710/ DOI: 10.1002/biof.2051

evidence_span

{"source_cache": "artifacts/coumarin-research/18210747.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e78df713d6bc2e34f13e80a0ef04c217a176b5d6082cbb28fa5a62464fcce842", "start_char": 0, "end_char": 1237, "text_sha256": "e78df713d6bc2e34f13e80a0ef04c217a176b5d6082cbb28fa5a62464fcce842"}

experimental_model

Cell viability, cell cycle, protein and mitochondrial assays

exposure

Coumarin; reported viability IC50 54.2 micromolar

limitations

Cultured cancer-cell response does not establish treatment efficacy; indexed abstract does not specify all exposure durations.

nutrient_topic

Coumarin research collection; topical membership is not evidence of a direct dietary effect. · Coumarin

organism

Human cell line

plain_language

A cell-death execution enzyme became active.

primary_references

[coumarin-p18210747] Coumarin induces cell cycle arrest and apoptosis in human cervical cancer HeLa cells through a mitochondria- and caspase-3 dependent mechanism and NF-kappaB down-regulation. (2007). https://pubmed.ncbi.nlm.nih.gov/18210747/

tissue_or_cell_type

HeLa cervical cancer cells

Coumarin: metabolism, signaling and nutrient connections (2026-09-17) · lines 397–408

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell viability, cell cycle, protein and mitochondrial assays · source_derived_draft · unverified_draft

### coumarin-hela-casp3 Coumarin activated caspase-3 in HeLa cells before apoptosis. Condition category: normal nutrient_topic: Coumarin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cell-death execution enzyme became active. organism: Human cell line tissue_or_cell_type: HeLa cervical cancer cells experimental_model: Cell viability, cell cycle, protein and mitochondrial assays limitations: Cultured cancer-cell response does not establish treatment efficacy; indexed abstract does not specify all exposure durations. exposure: Coumarin; reported viability IC50 54.2 micromolar evidence_span: {"source_cache": "artifacts/coumarin-research/18210747.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e78df713d6bc2e34f13e80a0ef04c217a176b5d6082cbb28fa5a62464fcce842", "start_char": 0, "end_char": 1237, "text_sha256": "e78df713d6bc2e34f13e80a0ef04c217a176b5d6082cbb28fa5a62464fcce842"} [coumarin-p18210747] Coumarin induces cell cycle arrest and apoptosis in human cervical cancer HeLa cells through a mitochondria- and caspase-3 dependent mechanism and NF-kappaB down-regulation. (2007). https://pubmed.ncbi.nlm.nih.gov/18210747/

duration

Not stated here

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

experimental_model

Human HepG2 hepatoma cells

exposure

Lariciresinol, dose-dependent

limitations

The enantiomer is not stated, and the abstract does not give the concentration range or the inhibitory concentration.

organism

Human HepG2 hepatoma cells

plain_language

Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot.

primary_references

Lariciresinol induces apoptosis in HepG2 cells via mitochondrial-mediated apoptosis pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29247613/ DOI: 10.1016/j.ejphar.2017.12.015

route

In vitro

tissue

Mitochondrial membrane potential and apoptosis-associated proteins

Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 209–218

Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

## lariciresinol-lowers-mitochondrial-membrane-potential Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot. Model/species: Human HepG2 hepatoma cells Tissue/system: Mitochondrial membrane potential and apoptosis-associated proteins Exposure: Lariciresinol, dose-dependent Route: In vitro Duration: Not stated here Limits: The enantiomer is not stated, and the abstract does not give the concentration range or the inhibitory concentration. Primary reference: Lariciresinol induces apoptosis in HepG2 cells via mitochondrial-mediated apoptosis pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29247613/ DOI: 10.1016/j.ejphar.2017.12.015 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

evidence_span

{"source_cache": "artifacts/dihydrocapsaicin-research/29035676.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98", "start_char": 0, "end_char": 2035, "text_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98"}

experimental_model

Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays

exposure

Dihydrocapsaicin against cardiopulmonary resuscitation alone and against body surface cooling

limitations

Proposes the central mechanism and measures each step, but with six animals per group and immunohistochemical rather than functional readouts.

nutrient_topic

Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

organism

Rat

plain_language

Fewer brain cells died, by about as much as physical cooling achieved.

primary_references

[dhc-p29035676] The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29035676/ DOI: 10.1089/ther.2017.0032

tissue_or_cell_type

Hypothalamus, ventral septum and cerebral cortex

Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 439–450

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays · source_derived_draft · unverified_draft

### dhc-fewer-apoptotic-cells Neurological deficit scores in the dihydrocapsaicin group were significantly higher than in the cardiopulmonary resuscitation and body surface cooling groups, and there were significantly fewer apoptotic cells in the dihydrocapsaicin and body surface cooling groups than in the resuscitation group. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Fewer brain cells died, by about as much as physical cooling achieved. organism: Rat tissue_or_cell_type: Hypothalamus, ventral septum and cerebral cortex experimental_model: Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays limitations: Proposes the central mechanism and measures each step, but with six animals per group and immunohistochemical rather than functional readouts. exposure: Dihydrocapsaicin against cardiopulmonary resuscitation alone and against body surface cooling evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/29035676.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98", "start_char": 0, "end_char": 2035, "text_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98"} [dhc-p29035676] The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29035676/ DOI: 10.1089/ther.2017.0032

evidence_span

{"source_cache": "artifacts/dihydrocapsaicin-research/27748914.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90", "start_char": 0, "end_char": 1610, "text_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90"}

experimental_model

U251 human glioma cells with flow cytometry, transmission electron microscopy and a murine xenograft model

exposure

Capsaicin and dihydrocapsaicin applied across doses and times, with L929 normal fibroblasts as a selectivity control

limitations

Includes a normal-cell control and an in vivo arm. Cell-line concentrations are not stated in the abstract and are not assumed here.

nutrient_topic

Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

organism

Human cells and mouse

plain_language

It kills glioma cells through the mitochondria while largely sparing normal cells.

primary_references

[dhc-p27748914] Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+‑mediated mitochondrial pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27748914/ DOI: 10.3892/mmr.2016.5784

tissue_or_cell_type

Glioma cells

Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 712–723

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · U251 human glioma cells with flow cytometry, transmission electron microscopy and a murine xenograft model · source_derived_draft · unverified_draft

### dhc-glioma-apoptosis Treatment of U251 glioma cells with capsaicin and dihydrocapsaicin resulted in a dose- and time-dependent inhibition of cell viability and induction of apoptosis, whereas few effects were observed on the viability of L929 normal murine fibroblast cells, and the apoptosis was associated with generation of reactive oxygen species, increased calcium concentrations, mitochondrial depolarization, release of cytochrome c into the cytosol and activation of caspase-9 and caspase-3, with anti-tumour effects confirmed in a murine tumour xenograft model. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: It kills glioma cells through the mitochondria while largely sparing normal cells. organism: Human cells and mouse tissue_or_cell_type: Glioma cells experimental_model: U251 human glioma cells with flow cytometry, transmission electron microscopy and a murine xenograft model limitations: Includes a normal-cell control and an in vivo arm. Cell-line concentrations are not stated in the abstract and are not assumed here. exposure: Capsaicin and dihydrocapsaicin applied across doses and times, with L929 normal fibroblasts as a selectivity control evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/27748914.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90", "start_char": 0, "end_char": 1610, "text_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90"} [dhc-p27748914] Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+‑mediated mitochondrial pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27748914/ DOI: 10.3892/mmr.2016.5784

evidence_span

{"source_cache": "artifacts/mebendazole-research/30414098.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400", "start_char": 0, "end_char": 1743, "text_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400"}

experimental_model

Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice

exposure

Mebendazole alone and combined with radiation

limitations

A combination study in one meningioma line and one implanted model. The mechanism is inferred from immunohistochemistry rather than dissected.

nutrient_topic

Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

organism

Human cells and mouse

plain_language

Added to radiation it killed more tumour cells than radiation alone.

primary_references

[mbz-p30414098] Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma. (2018). https://pubmed.ncbi.nlm.nih.gov/30414098/ DOI: 10.1007/s11060-018-03009-7

tissue_or_cell_type

Malignant meningioma

Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 563–574

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice · source_derived_draft · unverified_draft

### mbz-adds-to-radiation In meningioma cell lines the half-maximal inhibitory concentration for mebendazole was 0.26 to 0.42 micromolar, mebendazole alone induced cytotoxicity but the combination with radiation gave a greater reduction in colony formation and higher levels of cleaved caspase-3, and in mice implanted intracranially with human meningioma both mebendazole alone and the combination gave a survival benefit with increased apoptosis and decreased tumour cell and vascular proliferation. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: Added to radiation it killed more tumour cells than radiation alone. organism: Human cells and mouse tissue_or_cell_type: Malignant meningioma experimental_model: Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice limitations: A combination study in one meningioma line and one implanted model. The mechanism is inferred from immunohistochemistry rather than dissected. exposure: Mebendazole alone and combined with radiation evidence_span: {"source_cache": "artifacts/mebendazole-research/30414098.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400", "start_char": 0, "end_char": 1743, "text_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400"} [mbz-p30414098] Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma. (2018). https://pubmed.ncbi.nlm.nih.gov/30414098/ DOI: 10.1007/s11060-018-03009-7