Evidence map›Paper›PMID 31575959›Full record

ArticleScientific reports2019

Mitigation of radiation-induced gastro-intestinal injury by the polyphenolic acetate 7, 8-diacetoxy-4-methylthiocoumarin in mice.

Kavya Venkateswaran, Anju Shrivastava, Paban K Agrawala, Ashok K Prasad, Sagolsem Chandrika Devi, Kailash Manda, Virinder S Parmar, Bilikere S Dwarakanath

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Irradiation-Induced Intestinal Damage Is Recovered by the Indigenous Gut BacteriaFrontiers in cellular and infection microbiology · 2020
    Article
  11. Methamphetamine Induces Intestinal Inflammatory Injury via Nod-Like Receptor 3 Protein (NLRP3) Inflammasome Overexpression In Vitro and In Vivo.Medical science monitor : international medical journal of experimental and clinical research · 2019
    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 3 institutions in 2 countries.

Kavya VenkateswaranDivision of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Marg, Lucknow Road, Delhi, 110054, India.
Anju ShrivastavaDepartment of Zoology, University of Delhi, Delhi, 110007, India.
Paban K AgrawalaDivision of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Marg, Lucknow Road, Delhi, 110054, India.
Ashok K PrasadBioorganic Laboratory, Department of Chemistry, University of Delhi, Delhi, 110007, India.
Sagolsem Chandrika DeviDivision of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Marg, Lucknow Road, Delhi, 110054, India.
Kailash MandaDivision of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Marg, Lucknow Road, Delhi, 110054, India.
Virinder S ParmarBioorganic Laboratory, Department of Chemistry, University of Delhi, Delhi, 110007, India.
Bilikere S DwarakanathDivision of Metabolic Cell Signalling Research, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Marg, Lucknow Road, Delhi, 110054, India. dwarakanath@sphic.org.cn.
Institute of Nuclear Medicine & Allied Sciences · INUniversity of Delhi · INMedgar Evers College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation-induced intestinal injury (RIII) constitutes a crucial clinical element of acute radiation syndrome with life-threatening implications posing challenges in devising effective medical countermeasures. Herein, we report the potential of 7, 8-diacetoxy-4-methylthiocoumarin (DAMTC) to mitigate RIII following total-body irradiation (TBI) in C57BL/6 mice and underlying mechanisms. Administration of DAMTC 24 hours post TBI facilitated structural reconstitution and restoration of functional absorption linked to alleviation of radiation-induced apoptotic death of intestinal crypt progenitor/stem (ICPS) and villus stromal cells through induction of Bcl-2 family-mediated anti-apoptotic signalling. Reduction in TBI-induced DNA damage accumulation coupled with inhibition of cell cycle arrest through stimulation of anti-p53- and anti-p21-dependent synergistic signalling protected ICPS cells from radiation injury. Enhanced proliferation of crypt stem cells, induction of anti-oxidant defence, subjugation of TBI-induced lipid peroxidation and phenotypic polarization of intestinal macrophages to anti-inflammatory M2 class underlie amelioration of RIII. Stimulation of multiple mitigative signalling processes by DAMTC appeared to be associated with enhanced protein acetylation, an important regulator of cellular responses to radiation damage. Our findings establish the mitigative potential of DAMTC against RIII by hyper-acetylation-mediated epigenetic regulation, which triggers axes of anti-apoptotic and pro-survival pathways, enabling proliferation and maintenance of ICPS cells leading to epithelial regeneration.

Indexed as

Abnormalities, Radiation-InducedAcute Radiation SyndromeAnimalsCell ProliferationCoumarinsFemaleGastrointestinal TractInflammationLipid PeroxidationMacrophagesMiceMice, Inbred C57BLSignal TransductionStromal CellsWhole-Body IrradiationcoumarinCoumarins

Identifiers

PMID31575959
PMCPMC6773728
OpenAlexW2978785618

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.