Evidence map›Paper›PMID 31950223›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Pantoprazole abrogated cisplatin-induced nephrotoxicity in mice via suppression of inflammation, apoptosis, and oxidative stress.

Raed S Ismail, Mohammed S El-Awady, Memy H Hassan

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
  2. Article
  3. Renoprotective Effects of Brown-StrainInternational journal of molecular sciences · 2024
    Article
  4. Review
  5. Article
  6. Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Nephrotoxicity in cancer treatment: An update.Advances in cancer research · 2022
    Article
  10. Article
  11. Review
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 3 countries.

Raed S IsmailDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azahr University, Cairo, Egypt.
Mohammed S El-AwadyDepartment of Pharmacology and Toxicology, College of Pharmacy, Taibah University, Al-Madinah Al-Munawara, Saudi Arabia.
Memy H HassanDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azahr University, Cairo, Egypt. memymahmoud@yahoo.com.ORCID https://orcid.org/0000-0002-3957-2343
Al-Azhar University · EGMansoura University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current study was designed to evaluate the potential abatement effect of pantoprazole against cisplatin-induced nephrotoxicity and establishing the possible protective mechanisms. Thirty-two male mice were allocated for treatment with saline, single dose of cisplatin (10 mg/kg/i.p), pantoprazole (30 mg/kg/once daily) for 5 days or combination of pantoprazole and cisplatin for 5 days. Urine, blood, and both kidneys were collected for further evaluations. Pantoprazole significantly countermand cisplatin-induced disfigurement of renal histology, kidney weight to body weight ratio, serum levels of creatinine and urea, and microalbuminuria. Furthermore, pantoprazole mostly normalized cisplatin-induced distortion of renal levels of inflammatory cytokines (tumor necrosis factor-alpha, interleukin-6, interleukin-10) and renal content of apoptosis regulating protein expressions (Bax, Bcl2, and active caspase 3). In addition, pantoprazole significantly subsided cisplatin-induced distortion of renal lipid peroxidation marker (MDA), renal superoxide dismutase, and catalase activities and renal reduced glutathione content. This study provides an evidence for the protective utility of short-term pantoprazole against cisplatin-induced nephrotoxicity in mice. The protective mechanism of pantoprazole could be through diminution of cisplatin-induced inflammation, oxidative stress, and their subsequent apoptotic renal cell death via abatement of apoptosis regulating protein expressions (Bax, Bcl2, and active caspase3).

Indexed as

AnimalsAntineoplastic AgentsApoptosisbcl-2-Associated X ProteinCaspase 3CisplatinCytokinesInflammationKidney DiseasesLipid PeroxidationMaleMiceOxidative StressPantoprazoleProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsBax protein, mousebcl-2-Associated X ProteinBcl2 protein, mouseCasp3 protein, mouseCaspase 3CisplatinCytokinesPantoprazoleProto-Oncogene Proteins c-bcl-2ApoptosisCisplatinInflammationNephrotoxicityOxidative stressPantoprazole

Identifiers

PMID31950223
OpenAlexW3000325092

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.