Skip to content

Study · Animal study (in vivo) · 2011

9 results

Oxytocin inhibits NADPH oxidase and P38 MAPK in cisplatin-induced nephrotoxicity.

Rashed LA, Hashem RM, Soliman HM

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie27 Aug 2011Cited by 58 (Europe PMC)

PMID21993003 (opens in a new tab)DOI10.1016/j.biopha.2011.07.001 (opens in a new tab)PepBankPUB-21993003
Publisher pagePubMedAsk about this study
Jump to 9 results

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study9

9 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin significantly decreased NADPH oxidase gene expression.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin lowered activity of the NADPH oxidase gene.

    Peptide
    Oxytocin
    Outcome
    DecreaseNADPH oxidase gene expression
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin significantly decreased P38 MAPK gene expression.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin lowered activity of the P38 MAPK gene.

    Peptide
    Oxytocin
    Outcome
    DecreaseP38 MAPK gene expression
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin significantly decreased nitric oxide.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin lowered nitric oxide.

    Peptide
    Oxytocin
    Outcome
    DecreaseNitric oxide
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin significantly decreased myeloperoxidase.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin lowered myeloperoxidase.

    Peptide
    Oxytocin
    Outcome
    DecreaseMyeloperoxidase
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin significantly decreased TBARS.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin lowered TBARS, a marker of oxidative damage.

    Peptide
    Oxytocin
    Outcome
    DecreaseTBARS
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin increased renal tissue levels of reduced glutathione.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin raised kidney glutathione, an antioxidant.

    Peptide
    Oxytocin
    Outcome
    IncreaseRenal reduced glutathione
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin increased renal tissue levels of superoxide dismutase.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin raised kidney superoxide dismutase, an antioxidant enzyme.

    Peptide
    Oxytocin
    Outcome
    IncreaseRenal superoxide dismutase
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of OT significantly decreased the gene expression of both NADPH oxidase and P38 MAPK, nitric oxide (NO), myloperoxidase (MPO), and TBARS, furthermore it increased the renal tissue levels of antioxidants; reduced glutathione (GSH), and superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin reduced monocellular infiltration in kidney histology.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin reduced immune cell build-up in kidney tissue.

    Peptide
    Oxytocin
    Outcome
    DecreaseMonocellular infiltration (histology)
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Histologically, OT reduced the monocellular infiltration as well as the tubular damage in CP-induced nephrotoxicity.
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In an animal model of cisplatin-induced nephrotoxicity, oxytocin reduced tubular damage in kidney histology.

    In plain wordsIn an animal model of cisplatin kidney injury, oxytocin reduced damage to kidney tubules.

    Peptide
    Oxytocin
    Outcome
    DecreaseTubular damage (histology)
    Study

    n: not reported in source

    Cisplatin-induced nephrotoxicity
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Histologically, OT reduced the monocellular infiltration as well as the tubular damage in CP-induced nephrotoxicity.
    1 context sentence
    Summary · context
    We mainly aimed to study the protective effect of oxytocin (OT) on CP-induced nephrotoxicity whereas; it was previously shown to have anti-inflammatory effects in different inflammation models.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    11 Oct 2026, 01:30 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.