Evidence map›Paper›PMID 35902739›Full record

ArticleScientific reports2022

Cytoprotective effect of genistein against dexamethasone-induced pancreatic β-cell apoptosis.

Kanchana Suksri, Namoiy Semprasert, Thawornchai Limjindaporn, Pa-Thai Yenchitsomanus, Sirirat Kooptiwoot, Suwattanee Kooptiwut

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.4field-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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Genistein: a promising modulator of apoptosis and survival signaling in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  7. Review
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

6 authors at 2 institutions in 1 country.

Kanchana SuksriDivision of Endocrinology, Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Namoiy SemprasertDivision of Endocrinology, Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Thawornchai LimjindapornDepartment of Anatomy, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Pa-Thai YenchitsomanusDivision of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Sirirat KooptiwootDepartment of Psychiatry, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Suwattanee KooptiwutDivision of Endocrinology, Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand. S_kooptiwut@hotmail.com.
Siriraj Hospital · THMahidol University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Steroid-induced diabetes is a well-known metabolic side effect of long-term use of glucocorticoid (GC). Our group recently demonstrated dexamethasone-induced pancreatic β-cell apoptosis via upregulation of TRAIL and TRAIL death receptor (DR5). Genistein protects against pancreatic β-cell apoptosis induced by toxic agents. This study aimed to investigate the cytoprotective effect of genistein against dexamethasone-induced pancreatic β-cell apoptosis in cultured rat insulinoma (INS-1) cell line and in isolated mouse islets. In the absence of genistein, dexamethasone-induced pancreatic β-cell apoptosis was associated with upregulation of TRAIL, DR5, and superoxide production, but downregulation of TRAIL decoy receptor (DcR1). Dexamethasone also activated the expression of extrinsic and intrinsic apoptotic proteins, including Bax, NF-κB, caspase-8, and caspase-3, but suppressed the expression of the anti-apoptotic Bcl-2 protein. Combination treatment with dexamethasone and genistein protected against pancreatic β-cell apoptosis, and reduced the effects of dexamethasone on the expressions of TRAIL, DR5, DcR1, superoxide production, Bax, Bcl-2, NF-κB, caspase-8, and caspase-3. Moreover, combination treatment with dexamethasone and genistein reduced the expressions of TRAIL and DR5 in isolated mouse islets. The results of this study demonstrate the cytoprotective effect of genistein against dexamethasone-induced pancreatic β-cell apoptosis in both cell line and islets via reduced TRAIL and DR5 protein expression.

Indexed as

Receptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandAnimalsApoptosisApoptosis Regulatory Proteinsbcl-2-Associated X ProteinCaspase 3Caspase 8Cell Line, TumorDexamethasoneGenisteinMiceNF-kappa BProto-Oncogene Proteins c-bcl-2RatsSuperoxidesApoptosis Regulatory Proteinsbcl-2-Associated X ProteinCaspase 3Caspase 8DexamethasoneGenisteinNF-kappa BProto-Oncogene Proteins c-bcl-2Receptors, TNF-Related Apoptosis-Inducing LigandSuperoxidesTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID35902739
PMCPMC9334585
OpenAlexW4288435401

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.