Evidence map›Paper›PMID 33046085›Full record

ArticleReproductive biology and endocrinology : RB&E2020

Cyclosporin A protects JEG-3 cells against oxidative stress-induced apoptosis by inhibiting the p53 and JNK/p38 signaling pathways.

Bin He, Qi Yue Li, Yuan Yuan Wu, Jing Ling Ruan, Xiao Ming Teng, Da Jin Li, Chuan Ling Tang

Abstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. A real-world disproportionality analysis of cyclosporine from the FDA Adverse Event Reporting System (FAERS) database.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  5. Article
  6. 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

7 authors.

Bin HeDepartment of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 201204, China.
Qi Yue LiDepartment of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 201204, China.
Yuan Yuan WuDepartment of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 201204, China.
Jing Ling RuanDepartment of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 201204, China.
Xiao Ming TengDepartment of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 201204, China.
Da Jin LiLaboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200011, China.
Chuan Ling TangDepartment of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 201204, China. ttangirl56@sina.com.ORCID http://orcid.org/0000-0001-8724-2894

Funding

National Natural Science Foundation of China 81971383National Nature Science Foundation of China 81300505Natural Science Foundation of Shanghai 17ZR1422000
6 · The paper itself

Abstract

backgroundTrophoblast cells are required for the establishment of pregnancy and fetal development. Apoptosis is an essential feature for trophoblast invasion. Uncontrolled trophoblast apoptosis is related to some complicate pregnancies. Oxidative stress (OS) is an important inducer of trophoblast apoptosis. Cyclosporin A (CsA) has been shown to promote the activity of trophoblast cells and reduce OS-induced oxidative injury. We investigated the role and mechanism of CsA in oxidative stress-induced trophoblast cell apoptosis.

methodsJEG-3 cells were cocultured with H

resultsCsA increased the viability, alleviated morphological injury and reduced cell apoptosis of the H

conclusionsThese results suggested that CsA protected trophoblast cells from OS-induced apoptosis via the inhibition of the p53 and JNK/p38 signaling pathways.

Indexed as

ApoptosisCell Line, TumorCyclosporineCytoprotectionFemaleHumansMAP Kinase Signaling SystemOxidative Stressp38 Mitogen-Activated Protein KinasesPhosphorylationPregnancyProtective AgentsSignal TransductionTrophoblastsTumor Suppressor Protein p53Cyclosporinep38 Mitogen-Activated Protein KinasesProtective AgentsTumor Suppressor Protein p53ApoptosisMAPKOxidative stressp53Trophoblast

Identifiers

PMID33046085
PMCPMC7549196

What OpenQuestion holds

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LicenceCC BY
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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.