Evidence map›Paper›PMID 25197333›Full record

ArticleInternational journal of clinical and experimental pathology2014

Epigallocatechin-3-gallate protects against cisplatin nephrotoxicity by inhibiting the apoptosis in mouse.

Peimei Zou, Jian Song, Bei Jiang, Fei Pei, Binbin Chen, Xiangdong Yang, Guangyi Liu, Zhao Hu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

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  17. Plant-Derived Agents for Counteracting Cisplatin-Induced Nephrotoxicity.Oxidative medicine and cellular longevity · 2016
    Review
  18. Article
  19. Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells.Apoptosis : an international journal on programmed cell death · 2015
    Article
  20. 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

8 authors at 2 institutions in 1 country.

Peimei ZouDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Jian SongDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Bei JiangDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Fei PeiDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Binbin ChenDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Xiangdong YangDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Guangyi LiuDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China ; Ministry of Education Key Laboratory of Experimental Teratology and Institute of Molecular Medicine and Genetics, Shandong University School of Medicine Jinan, Shandong 250013, China.
Zhao HuDepartment of Nephrology, Qi Lu Hospital of Shandong University Jinan, Shandong 250012, China.
Qilu Hospital of Shandong University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin (CP) is a commonly used anticancer drug, but its notable side effect of nephrotoxicity limits its use in clinic. Epigallocatechin-3-gallate (EGCG), an anti-oxidant, anti-inflammatory, and anti-tumorigenic green tea polyphenol, has been available on the market for its beneficial effects. The aim of this study was to investigate whether EGCG can prevent the nephrotoxic effect of CP and the involved mechanisms. Male C57/BL6 mice were randomly divided into four groups: control group, EGCG group, CP group, and CP+EGCG group. On day 5, mice were sacrificed. Our results showed that EGCG treatment significantly ameliorated the histopathological changes and the increased serum creatinine and blood urea nitrogen (BUN) induced by CP. TUNEL-positive cells significantly reduced in the CP+EGCG group compared with CP group. EGCG also inhibited the expression of the ligand of death receptor Fas (Fas-L), apoptosis regulator BAX (Bax) and tumor-suppressor protein p53, and increased the expression of B-cell lymphoma 2 (Bcl-2). These findings suggest that EGCG can ameliorate CP-induced apoptosis in the kidney by regulating death receptor Fas conducted extrinsic pathway, and the expression of Bax and Bcl-2.

Indexed as

AnimalsAntineoplastic AgentsAntioxidantsApoptosisCatechinCisplatinDisease Models, AnimalKidneyKidney DiseasesMaleMiceMice, Inbred C57BLAntineoplastic AgentsAntioxidantsCatechinCisplatinepigallocatechin gallateapoptosisCisplatin (CP)Epigallocatechin-3-gallate (EGCG)mouserenal

Identifiers

PMID25197333
PMCPMC4152023
OpenAlexW2211842933

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.