Component

Apoptotic cell death

Apoptotic cell death. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. 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.

    Dihydrocapsaicin → Apoptotic cell death source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Combination therapy of low-dose dihydrocapsaicin and an ice pad significantly improved every measured outcome compared with monotherapies, achieving hypothermia faster by 28.6% than the ice pad, 350% than low-dose dihydrocapsaicin and 200% than high-dose dihydrocapsaicin alone, reducing neurological deficits by 63% against 26% with low-dose alone, reducing reactive oxygen species at 6 and 24 hours, increasing ATP by 42.9% against 25%, and decreasing apoptotic cell death by 48.5% against 24.9%.

    Hypothermia induced by a drug rather than by physical cooling → Hypothermia induced by physical means such as an ice pad or cold fluid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/30090648.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c", "start_char": 0, "end_char": 2110, "text_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c"}
    experimental_model
    Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion
    exposure
    Low-dose dihydrocapsaicin at 0.5 mg/kg or high-dose at 1.5 mg/kg, an ice pad at 31 degrees, and the combination, with an external-temperature-control arm
    limitations
    A large randomised design with a dose-response surprise: the high dose alone did nothing while the low dose worked. That non-monotonicity is recorded because it contradicts the simple dose-response in the other records.
    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
    Drug plus ice pack cooled faster and protected better than either on its own.
    primary_references
    [dhc-p30090648] Synergistically Induced Hypothermia and Enhanced Neuroprotection by Pharmacological and Physical Approaches in Stroke. (2018). https://pubmed.ncbi.nlm.nih.gov/30090648/ DOI: 10.14336/ad.2017.0817
    tissue_or_cell_type
    Brain

    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 335–346

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion · source_derived_draft · unverified_draft

    ### dhc-combination-beats-either Combination therapy of low-dose dihydrocapsaicin and an ice pad significantly improved every measured outcome compared with monotherapies, achieving hypothermia faster by 28.6% than the ice pad, 350% than low-dose dihydrocapsaicin and 200% than high-dose dihydrocapsaicin alone, reducing neurological deficits by 63% against 26% with low-dose alone, reducing reactive oxygen species at 6 and 24 hours, increasing ATP by 42.9% against 25%, and decreasing apoptotic cell death by 48.5% against 24.9%. 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: Drug plus ice pack cooled faster and protected better than either on its own. organism: Rat tissue_or_cell_type: Brain experimental_model: Randomised seven-group study in 144 male Sprague Dawley rats after middle cerebral artery occlusion limitations: A large randomised design with a dose-response surprise: the high dose alone did nothing while the low dose worked. That non-monotonicity is recorded because it contradicts the simple dose-response in the other records. exposure: Low-dose dihydrocapsaicin at 0.5 mg/kg or high-dose at 1.5 mg/kg, an ice pad at 31 degrees, and the combination, with an external-temperature-control arm evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/30090648.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c", "start_char": 0, "end_char": 2110, "text_sha256": "e688b4cd16fdd3847d8fe10113d243edf17839f32bef46fe85790a18ad6b920c"} [dhc-p30090648] Synergistically Induced Hypothermia and Enhanced Neuroprotection by Pharmacological and Physical Approaches in Stroke. (2018). https://pubmed.ncbi.nlm.nih.gov/30090648/ DOI: 10.14336/ad.2017.0817
    Complete structured claim and evidence

  2. Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin.

    Dihydrocapsaicin → The cGAS-STING pathway source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"}
    experimental_model
    Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation
    exposure
    Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation
    limitations
    The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence.
    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
    It protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes.
    primary_references
    [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167
    tissue_or_cell_type
    Skin flap vasculature

    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 699–710

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation · source_derived_draft · unverified_draft

    ### dhc-suppresses-sting Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin. 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 protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes. organism: Rat tissue_or_cell_type: Skin flap vasculature experimental_model: Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation limitations: The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence. exposure: Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"} [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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