Evidence map›Paper›PMID 26887929›Full record

ArticleScientific reports2016

Amelioration of intracellular stress and reduction of neural tube defects in embryos of diabetic mice by phytochemical quercetin.

Lixue Cao, Chengyu Tan, Fantong Meng, Peiyan Liu, E Albert Reece, Zhiyong Zhao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 43 citations in OpenAlex.

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  8. Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020
    Review
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  14. Formation of neurodegenerative aggresome and death-inducing signaling complex in maternal diabetes-induced neural tube defects.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Quercetin Isolated fromJournal of diabetes research · 2016
    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

6 authors at 2 institutions in 2 countries.

Lixue CaoDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Chengyu TanDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Fantong MengCollege of Marine Technology and Environment, Dalian Ocean University, Dalian, China.
Peiyan LiuDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
E Albert ReeceDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Zhiyong ZhaoDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
University of Maryland, Baltimore · USDalian Ocean University · CN

Funding

Protein Modifications and Unfolded Protein Response in Diabetic EmbryopathyR01HD076245 · NICHD · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHAO, ZHIYONG · 2013 to 2017
$1.6M
Targeting Nitrosative Stress to Prevent Fetal Anomalies in Diabetic EmbryopathyR03HD075995 · NICHD · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHAO, ZHIYONG · 2014 to 2015
$152k
NICHD NIH HHS R01 HD076245NICHD NIH HHS R01HD076245NICHD NIH HHS R03 HD075995NICHD NIH HHS R03HD075995
6 · The paper itself

Abstract

Diabetes mellitus in early pregnancy causes birth defects, including neural tube defects (NTDs). Hyperglycemia increases production of nitric oxide (NO) through NO synthase 2 (Nos2) and reactive oxygen species (ROS), generating nitrosative and oxidative stress conditions in the embryo. The present study aimed to target nitrosative stress using a naturally occurring Nos2 inhibitor, quercetin, to prevent NTDs in the embryos of diabetic mice. Daily administration of quercetin to diabetic pregnant mice during the hyperglycemia-susceptible period of organogenesis significantly reduced NTDs and cell apoptosis in the embryos, compared with those of vehicle-treated diabetic pregnant mice. Using HPLC-coupled ESI-MS/MS, quercetin metabolites, including methylated and sulfonylated derivatives, were detected in the conceptuses. The methylated metabolite, 3-O-methylquercetin, was shown to reduce ROS level in embryonic stem cells cultured in high glucose. Quercetin treatment decreased the levels of Nos2 expression, protein nitrosylation, and protein nitration, alleviating nitrosative stress. Quercetin increased the expression of superoxide dismutase 1 and 2, and reduced the levels of oxidative stress markers. Expression of genes of redox regulating enzymes and DNA damage repair factors was upregulated. Our study demonstrates that quercetin ameliorates intracellular stresses, regulates gene expression, and reduces embryonic malformations in diabetic pregnancy.

Indexed as

AnimalsApoptosisDiabetes Mellitus, ExperimentalFemaleMiceNeural Tube DefectsNitric Oxide Synthase Type IIOxidative StressPregnancyPregnancy in DiabeticsQuercetinSuperoxide DismutaseSuperoxide Dismutase-1Superoxide Dismutase 2Nitric Oxide Synthase Type IINos2 protein, mouseQuercetinSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Superoxide Dismutase 2

Identifiers

PMID26887929
PMCPMC4757833
OpenAlexW2296087638

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.