Component

Cisplatin

Context-specific entity; species, compartment and exposure are stated on each claim.

10 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

Where it participates (unsigned role)

  1. Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone.

    Indicaxanthin → Apoptosis in human HeLa cervical cancer cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls
    duration
    24 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human HeLa cervical cancer cells
    limitations
    Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Human HeLa cervical cancer cells
    plain_language
    Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone.
    primary_references
    The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
    route
    In vitro co-treatment
    tissue
    Cell death and redox assays

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 283–292

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft

    ## indicaxanthin-cisplatin-apoptosis Co-treatment with indicaxanthin increased cisplatin-associated apoptosis in HeLa cells relative to cisplatin alone. Model/species: Human HeLa cervical cancer cells Tissue: Cell death and redox assays Exposure: Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls Route: In vitro co-treatment Duration: 24 h Limits: Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  2. Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells.

    Indicaxanthin → Reduced glutathione-associated signal in human HeLa cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls
    duration
    24 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human HeLa cervical cancer cells
    limitations
    Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Glutathione was assessed with CMFDA fluorescence; the result does not establish an isolated block of synthesis.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Human HeLa cervical cancer cells
    plain_language
    Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells.
    primary_references
    The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
    route
    In vitro co-treatment
    tissue
    Cell death and redox assays

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 294–303

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft

    ## indicaxanthin-cisplatin-gsh Indicaxanthin plus cisplatin lowered the glutathione-associated signal more than cisplatin alone in HeLa cells. Model/species: Human HeLa cervical cancer cells Tissue: Cell death and redox assays Exposure: Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls Route: In vitro co-treatment Duration: 24 h Limits: Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Glutathione was assessed with CMFDA fluorescence; the result does not establish an isolated block of synthesis. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  3. Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment.

    Indicaxanthin → Viability of human HeLa cervical cancer cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 2, 5 or 10 micromolar plus a cisplatin concentration series
    duration
    24 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human HeLa cervical cancer cells
    limitations
    Lower indicaxanthin concentrations were examined in a separate viability experiment; do not transfer all high-dose mechanistic measurements to this range.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Human HeLa cervical cancer cells
    plain_language
    Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment.
    primary_references
    The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
    route
    In vitro co-treatment
    tissue
    Viability assay

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 316–325

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft

    ## indicaxanthin-cisplatin-low-dose Low-micromolar indicaxanthin enhanced the cisplatin-associated loss of HeLa-cell viability in a separate concentration-response experiment. Model/species: Human HeLa cervical cancer cells Tissue: Viability assay Exposure: Indicaxanthin 2, 5 or 10 micromolar plus a cisplatin concentration series Route: In vitro co-treatment Duration: 24 h Limits: Lower indicaxanthin concentrations were examined in a separate viability experiment; do not transfer all high-dose mechanistic measurements to this range. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  4. Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells.

    Indicaxanthin → Oxidant-sensitive fluorescence in human HeLa cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls
    duration
    24 h
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human HeLa cervical cancer cells
    limitations
    Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Human HeLa cervical cancer cells
    plain_language
    Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells.
    primary_references
    The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
    route
    In vitro co-treatment
    tissue
    Cell death and redox assays

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 305–314

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells · source_derived_draft · unverified_draft

    ## indicaxanthin-cisplatin-ros Indicaxanthin plus cisplatin increased oxidant-sensitive fluorescence more than cisplatin alone in HeLa cells. Model/species: Human HeLa cervical cancer cells Tissue: Cell death and redox assays Exposure: Indicaxanthin 60 micromolar with cisplatin 10 micromolar; individual-agent controls Route: In vitro co-treatment Duration: 24 h Limits: Cell-culture chemosensitization is not clinical cancer efficacy. Redox-probe signals and protein changes do not prove direct target binding. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  5. N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells.

    N-Acetyl-L-cysteine → Apoptosis in human HeLa cervical cancer cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    N-acetylcysteine 2 mM before indicaxanthin 60 micromolar plus cisplatin 10 micromolar
    duration
    NAC 1 h before the 24 h combination exposure
    evidence_access
    Primary open full text, relevant results/methods and PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human HeLa cervical cancer cells with NAC pretreatment
    limitations
    NAC blunted the combination response without restoring every outcome to baseline. This experiment is not a recommendation for or against NAC during chemotherapy.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Human HeLa cervical cancer cells with NAC pretreatment
    plain_language
    N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells.
    primary_references
    The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994
    route
    In vitro pretreatment/co-treatment
    tissue
    Cell death and redox assays

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 327–336

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Human HeLa cervical cancer cells with NAC pretreatment · source_derived_draft · unverified_draft

    ## indicaxanthin-nac-combination-antagonism N-acetylcysteine pretreatment reduced apoptosis caused by the indicaxanthin/cisplatin combination in HeLa cells. Model/species: Human HeLa cervical cancer cells with NAC pretreatment Tissue: Cell death and redox assays Exposure: N-acetylcysteine 2 mM before indicaxanthin 60 micromolar plus cisplatin 10 micromolar Route: In vitro pretreatment/co-treatment Duration: NAC 1 h before the 24 h combination exposure Limits: NAC blunted the combination response without restoring every outcome to baseline. This experiment is not a recommendation for or against NAC during chemotherapy. Primary reference: The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis. (2020). https://pubmed.ncbi.nlm.nih.gov/32630700/ DOI: 10.3390/biom10070994 Access: Primary open full text, relevant results/methods and PubMed metadata.
    Complete structured claim and evidence

  6. SAC attenuated cisplatin-associated losses of catalase, GPx and glutathione reductase activities in proximal and distal tubules.

    S-allyl-L-cysteine / SAC → Rat tubular CAT, GPx and GR activities during SAC/cisplatin exposure source_derived_draftungraded
    Experimental context and source evidence
    acting_entity
    s-allylcysteine
    dose
    SAC 25 mg/kg; cisplatin dose not retrieved
    duration
    Single SAC dose for signaling arm; timing not retrieved
    evidence_access
    Primary abstract
    experimental_comparison
    SAC with cisplatin versus cisplatin injury controls
    experimental_model
    Cisplatin-challenged renal cortex and isolated proximal/distal tubules
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    Isoforms were not resolved; activity preservation does not demonstrate selenium or riboflavin repletion.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Rattus norvegicus
    plain_language
    Several antioxidant activities were retained during injury.
    primary_references
    [24779924] S-allylcysteine prevents cisplatin-induced nephrotoxicity and oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24779924/ · DOI 10.1111/jphp.12263
    route
    Administration route not specified in accessed abstract
    tissue_or_cell_type
    Cisplatin-challenged renal cortex and isolated proximal/distal tubules

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 356–363

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cisplatin-challenged renal cortex and isolated proximal/distal tubules · source_derived_draft · unverified_draft

    ## s-allylcysteine-cisplatin-antioxidant-enzymes Several antioxidant activities were retained during injury. SAC attenuated cisplatin-associated losses of catalase, GPx and glutathione reductase activities in proximal and distal tubules. Model: Cisplatin-challenged renal cortex and isolated proximal/distal tubules Limitations: Isoforms were not resolved; activity preservation does not demonstrate selenium or riboflavin repletion. Evidence access: Primary abstract [24779924] S-allylcysteine prevents cisplatin-induced nephrotoxicity and oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24779924/ · DOI 10.1111/jphp.12263 Structured context: {"organism": "Rattus norvegicus", "tissue_or_cell_type": "Cisplatin-challenged renal cortex and isolated proximal/distal tubules", "dose": "SAC 25 mg/kg; cisplatin dose not retrieved", "duration": "Single SAC dose for signaling arm; timing not retrieved", "route": "Administration route not specified in accessed abstract", "experimental_comparison": "SAC with cisplatin versus cisplatin injury controls", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}
    Complete structured claim and evidence

  7. SAC attenuated cisplatin-associated increases in renal p47phox and gp91phox expression.

    S-allyl-L-cysteine / SAC → Rat renal p47phox/gp91phox abundance during SAC/cisplatin exposure source_derived_draftungraded
    Experimental context and source evidence
    acting_entity
    s-allylcysteine
    dose
    SAC 25 mg/kg; cisplatin dose not retrieved
    duration
    Single SAC dose for signaling arm; timing not retrieved
    evidence_access
    Primary abstract
    experimental_comparison
    SAC with cisplatin versus cisplatin injury controls
    experimental_model
    Cisplatin-challenged renal cortex and isolated proximal/distal tubules
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    Expression endpoints do not establish direct inhibition of the assembled NADPH oxidase.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Rattus norvegicus
    plain_language
    Components of a ROS-producing system changed.
    primary_references
    [24779924] S-allylcysteine prevents cisplatin-induced nephrotoxicity and oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24779924/ · DOI 10.1111/jphp.12263
    route
    Administration route not specified in accessed abstract
    tissue_or_cell_type
    Cisplatin-challenged renal cortex and isolated proximal/distal tubules

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 347–354

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cisplatin-challenged renal cortex and isolated proximal/distal tubules · source_derived_draft · unverified_draft

    ## s-allylcysteine-cisplatin-nox Components of a ROS-producing system changed. SAC attenuated cisplatin-associated increases in renal p47phox and gp91phox expression. Model: Cisplatin-challenged renal cortex and isolated proximal/distal tubules Limitations: Expression endpoints do not establish direct inhibition of the assembled NADPH oxidase. Evidence access: Primary abstract [24779924] S-allylcysteine prevents cisplatin-induced nephrotoxicity and oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24779924/ · DOI 10.1111/jphp.12263 Structured context: {"organism": "Rattus norvegicus", "tissue_or_cell_type": "Cisplatin-challenged renal cortex and isolated proximal/distal tubules", "dose": "SAC 25 mg/kg; cisplatin dose not retrieved", "duration": "Single SAC dose for signaling arm; timing not retrieved", "route": "Administration route not specified in accessed abstract", "experimental_comparison": "SAC with cisplatin versus cisplatin injury controls", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}
    Complete structured claim and evidence

  8. SAC 25 mg/kg attenuated the cisplatin-associated reduction of renal cortical Nrf2.

    S-allyl-L-cysteine / SAC → Rat Nrf2 / Nfe2l2 source_derived_draftungraded
    Experimental context and source evidence
    acting_entity
    s-allylcysteine
    dose
    SAC 25 mg/kg; cisplatin dose not retrieved
    duration
    Single SAC dose for signaling arm; timing not retrieved
    evidence_access
    Primary abstract
    experimental_comparison
    SAC with cisplatin versus cisplatin injury controls
    experimental_model
    Cisplatin-challenged renal cortex and isolated proximal/distal tubules
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    Renal protection does not establish preserved antitumor activity or a safe patient combination.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Rattus norvegicus
    plain_language
    A drug-injury model showed preservation of a defense regulator.
    primary_references
    [24779924] S-allylcysteine prevents cisplatin-induced nephrotoxicity and oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24779924/ · DOI 10.1111/jphp.12263
    route
    Administration route not specified in accessed abstract
    tissue_or_cell_type
    Cisplatin-challenged renal cortex and isolated proximal/distal tubules

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 338–345

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cisplatin-challenged renal cortex and isolated proximal/distal tubules · source_derived_draft · unverified_draft

    ## s-allylcysteine-cisplatin-nrf2 A drug-injury model showed preservation of a defense regulator. SAC 25 mg/kg attenuated the cisplatin-associated reduction of renal cortical Nrf2. Model: Cisplatin-challenged renal cortex and isolated proximal/distal tubules Limitations: Renal protection does not establish preserved antitumor activity or a safe patient combination. Evidence access: Primary abstract [24779924] S-allylcysteine prevents cisplatin-induced nephrotoxicity and oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24779924/ · DOI 10.1111/jphp.12263 Structured context: {"organism": "Rattus norvegicus", "tissue_or_cell_type": "Cisplatin-challenged renal cortex and isolated proximal/distal tubules", "dose": "SAC 25 mg/kg; cisplatin dose not retrieved", "duration": "Single SAC dose for signaling arm; timing not retrieved", "route": "Administration route not specified in accessed abstract", "experimental_comparison": "SAC with cisplatin versus cisplatin injury controls", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}
    Complete structured claim and evidence

  9. Gavage with 6-gingerol reduced kaolin ingestion after cisplatin administration in rats.

    6-Gingerol → Cisplatin-associated kaolin ingestion in rats source_derived_draftungraded
    Experimental context and source evidence
    dose
    6-Gingerol 50 or 100 mg/kg twice; cisplatin 6 mg/kg once, 1 h after first gingerol dose
    duration
    Gingerol at 07:00 and 19:00; assessment 24 h after cisplatin
    evidence_access
    Primary PubMed abstract.
    evidence_scope
    literature_reviewed; model-specific source-derived curation, not universally established human effects
    experimental_model
    Rats in a cisplatin-induced pica model
    limitations
    Rats do not vomit; pica is a surrogate. This experiment does not establish human antiemetic efficacy or preserved anticancer efficacy.
    nutrient_topic
    Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
    organism
    Rats in a cisplatin-induced pica model
    plain_language
    Gavage with 6-gingerol reduced kaolin ingestion after cisplatin administration in rats.
    primary_references
    [6]-Gingerol Ameliorates Cisplatin-Induced Pica by Regulating the TPH/MAO-A/SERT/5-HT/5-HT3 Receptor System in Rats. (2020). https://pubmed.ncbi.nlm.nih.gov/33061309/ DOI: 10.2147/DDDT.S270185
    route
    Gingerol gavage; cisplatin intraperitoneal injection
    tissue
    Kaolin intake, ileum, medulla oblongata and serum

    Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 536–545

    Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Rats in a cisplatin-induced pica model · source_derived_draft · unverified_draft

    ## gingerols-6-cisplatin-pica Gavage with 6-gingerol reduced kaolin ingestion after cisplatin administration in rats. Model/species: Rats in a cisplatin-induced pica model Tissue: Kaolin intake, ileum, medulla oblongata and serum Exposure: 6-Gingerol 50 or 100 mg/kg twice; cisplatin 6 mg/kg once, 1 h after first gingerol dose Route: Gingerol gavage; cisplatin intraperitoneal injection Duration: Gingerol at 07:00 and 19:00; assessment 24 h after cisplatin Limits: Rats do not vomit; pica is a surrogate. This experiment does not establish human antiemetic efficacy or preserved anticancer efficacy. Primary reference: [6]-Gingerol Ameliorates Cisplatin-Induced Pica by Regulating the TPH/MAO-A/SERT/5-HT/5-HT3 Receptor System in Rats. (2020). https://pubmed.ncbi.nlm.nih.gov/33061309/ DOI: 10.2147/DDDT.S270185 Access: Primary PubMed abstract.
    Complete structured claim and evidence

  10. 6-Gingerol treatment attenuated the cisplatin-associated rise in measured serotonin in rats.

    6-Gingerol → Serotonin elevation in cisplatin-exposed rats source_derived_draftungraded
    Experimental context and source evidence
    dose
    6-Gingerol 50 or 100 mg/kg twice; cisplatin 6 mg/kg once, 1 h after first gingerol dose
    duration
    Gingerol at 07:00 and 19:00; assessment 24 h after cisplatin
    evidence_access
    Primary PubMed abstract.
    evidence_scope
    literature_reviewed; model-specific source-derived curation, not universally established human effects
    experimental_model
    Rats in a cisplatin-induced pica model
    limitations
    Rats do not vomit; pica is a surrogate. This experiment does not establish human antiemetic efficacy or preserved anticancer efficacy.
    nutrient_topic
    Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
    organism
    Rats in a cisplatin-induced pica model
    plain_language
    6-Gingerol treatment attenuated the cisplatin-associated rise in measured serotonin in rats.
    primary_references
    [6]-Gingerol Ameliorates Cisplatin-Induced Pica by Regulating the TPH/MAO-A/SERT/5-HT/5-HT3 Receptor System in Rats. (2020). https://pubmed.ncbi.nlm.nih.gov/33061309/ DOI: 10.2147/DDDT.S270185
    route
    Gingerol gavage; cisplatin intraperitoneal injection
    tissue
    Kaolin intake, ileum, medulla oblongata and serum

    Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 547–556

    Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Rats in a cisplatin-induced pica model · source_derived_draft · unverified_draft

    ## gingerols-6-cisplatin-serotonin 6-Gingerol treatment attenuated the cisplatin-associated rise in measured serotonin in rats. Model/species: Rats in a cisplatin-induced pica model Tissue: Kaolin intake, ileum, medulla oblongata and serum Exposure: 6-Gingerol 50 or 100 mg/kg twice; cisplatin 6 mg/kg once, 1 h after first gingerol dose Route: Gingerol gavage; cisplatin intraperitoneal injection Duration: Gingerol at 07:00 and 19:00; assessment 24 h after cisplatin Limits: Rats do not vomit; pica is a surrogate. This experiment does not establish human antiemetic efficacy or preserved anticancer efficacy. Primary reference: [6]-Gingerol Ameliorates Cisplatin-Induced Pica by Regulating the TPH/MAO-A/SERT/5-HT/5-HT3 Receptor System in Rats. (2020). https://pubmed.ncbi.nlm.nih.gov/33061309/ DOI: 10.2147/DDDT.S270185 Access: Primary PubMed abstract.
    Complete structured claim and evidence

In the sources

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