Evidence map›Paper›PMID 25595578›Full record

ArticleAmerican journal of obstetrics and gynecology2015

Curcumin ameliorates high glucose-induced neural tube defects by suppressing cellular stress and apoptosis.

Yanqing Wu, Fang Wang, E Albert Reece, Peixin Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of obstetrics and gynecology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-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

39 citing papers in PubMed, 74 citations in OpenAlex.

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  9. The Multifaced Actions of Curcumin in Pregnancy Outcome.Antioxidants (Basel, Switzerland) · 2021
    Review
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  16. Trehalose restores functional autophagy suppressed by high glucose.Reproductive toxicology (Elmsford, N.Y.) · 2019
    Article
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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

4 authors at 1 institution in 2 countries.

Yanqing WuProvincial Key Laboratory for Developmental Biology and Neurosciences, College of Life Sciences, Fujian Normal University, Fuzhou, People's Republic of China; Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD.
Fang WangDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD.
E Albert ReeceDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD.
Peixin YangDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD. Electronic address: pyang@upi.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Apoptotic Mechanism of Maternal Diabetes-Induced Neural Tube DefectsR01DK083243 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2010 to 2019
$3.1M
Molecular Signalling Pathways and Cellular Stress in Diabetic EmbryopathyR01DK103024 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI REECE, E. ALBERT, YANG, PEIXIN · 2014 to 2017
$1.7M
Autophagy and its Regulation in Diabetic EmbryopathyR01DK101972 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2014 to 2017
$1.6M
Metabolic Cellular Stress and its Regulatory Mechanism in Diabetic EmbryopathyR56DK095380 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2012 to 2012
$150k
NIDDK NIH HHS R01 DK083243NIDDK NIH HHS R01DK083243NIDDK NIH HHS R01 DK101972NIDDK NIH HHS R01DK101972NIDDK NIH HHS R01 DK103024NIDDK NIH HHS R01DK103024NIDDK NIH HHS R56 DK095380
6 · The paper itself

Abstract

objectiveCurcumin is a naturally occurring polyphenol present in the roots of the Curcuma longa plant (turmeric), which possesses antioxidant, antitumorigenic, and antiinflammatory properties. Here, we test whether curcumin treatment reduces high glucose-induced neural tube defects (NTDs), and if this occurs via blocking cellular stress and caspase activation. STUDY

designEmbryonic day 8.5 mouse embryos were collected for use in whole-embryo culture under normal (100 mg/dL) or high (300 mg/dL) glucose conditions, with or without curcumin treatment. After 24 hours in culture, protein levels of oxidative stress makers, nitrosative stress makers, endoplasmic reticulum (ER) stress makers, cleaved caspase 3 and 8, and the level of lipid peroxides were determined in the embryos. After 36 hours in culture, embryos were examined for evidence of NTD formation.

resultsAlthough 10 μmol/L of curcumin did not significantly reduce the rate of NTDs caused by high glucose, 20 μmol/L of curcumin significantly ameliorated high glucose-induced NTD formation. Curcumin suppressed oxidative stress in embryos cultured under high glucose conditions. Treatment reduced the levels of the lipid peroxidation marker, 4-hydroxynonenal, nitrotyrosine-modified protein, and lipid peroxides. Curcumin also blocked ER stress by inhibiting phosphorylated protein kinase RNA-like ER kinase, phosphorylated inositol-requiring protein-1α (p-IRE1α), phosphorylated eukaryotic initiation factor 2α (p-eIF2α), C/EBP-homologous protein, binding immunoglobulin protein, and x-box binding protein 1 messenger RNA splicing. Additionally, curcumin abolished caspase 3 and caspase 8 cleavage in embryos cultured under high glucose conditions.

conclusionCurcumin reduces high glucose-induced NTD formation by blocking cellular stress and caspase activation, suggesting that curcumin supplements could reduce the negative effects of diabetes on the embryo. Further investigation will be needed to determine if the experimental findings can translate into clinical settings.

Indexed as

AnimalsApoptosisCaspase 3Cell Physiological PhenomenaCurcuminEndoplasmic Reticulum StressGlucoseMiceMice, Inbred C57BLNeural Tube DefectsOxidative StressCaspase 3CurcuminGlucosecaspase activationcurcuminendoplasmic reticulum stresshigh glucoseneural tube defectsnitrosative stressoxidative stress

Identifiers

PMID25595578
PMCPMC4457597
OpenAlexW2072994145

What OpenQuestion holds

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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.