Evidence map›Paper›PMID 24628444›Full record

ArticleClinical and experimental immunology2014

Curcumin ameliorates autoimmune diabetes. Evidence in accelerated murine models of type 1 diabetes.

C N Castro, A E Barcala Tabarrozzi, J Winnewisser, M L Gimeno, M Antunica Noguerol, A C Liberman, D A Paz, R A Dewey, M J Perone

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-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

31 citing papers in PubMed, 83 citations in OpenAlex.

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  12. Immunomodulatory Effects and Mechanisms ofFrontiers in pharmacology · 2021
    Review
  13. Review
  14. Glucose transporters in brain in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
  15. Curcumin Attenuates Both Acute and Chronic Immune Nephritis.International journal of molecular sciences · 2020
    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

9 authors at 3 institutions in 1 country.

C N CastroInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
A E Barcala Tabarrozzi
J Winnewisser
M L Gimeno
M Antunica Noguerol
A C Liberman
D A Paz
R A Dewey
M J Perone
Biomedicine Research Institute of Buenos Aires - CONICET - Partner Institute of the Max Planck Society · ARInstituto Tecnológico de Chascomús · ARUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1DM) is a T cell-mediated autoimmune disease that selectively destroys pancreatic β cells. The only possible cure for T1DM is to control autoimmunity against β cell-specific antigens. We explored whether the natural compound curcumin, with anti-oxidant and anti-inflammatory activities, might down-regulate the T cell response that destroys pancreatic β cells to improve disease outcome in autoimmune diabetes. We employed two accelerated autoimmune diabetes models: (i) cyclophosphamide (CYP) administration to non-obese diabetic (NOD) mice and (ii) adoptive transfer of diabetogenic splenocytes into NODscid mice. Curcumin treatment led to significant delay of disease onset, and in some instances prevented autoimmune diabetes by inhibiting pancreatic leucocyte infiltration and preserving insulin-expressing cells. To investigate the mechanisms of protection we studied the effect of curcumin on key immune cell populations involved in the pathogenesis of the disease. Curcumin modulates the T lymphocyte response impairing proliferation and interferon (IFN)-γ production through modulation of T-box expressed in T cells (T-bet), a key transcription factor for proinflammatory T helper type 1 (Th1) lymphocyte differentiation, both at the transcriptional and translational levels. Also, curcumin reduces nuclear factor (NF)-κB activation in T cell receptor (TCR)-stimulated NOD lymphocytes. In addition, curcumin impairs the T cell stimulatory function of dendritic cells with reduced secretion of proinflammatory cytokines and nitric oxide (NO) and low surface expression of co-stimulatory molecules, leading to an overall diminished antigen-presenting cell activity. These in-vitro effects correlated with ex-vivo analysis of cells obtained from curcumin-treated mice during the course of autoimmune diabetes. These findings reveal an effective therapeutic effect of curcumin in autoimmune diabetes by its actions on key immune cells responsible for β cell death.

Indexed as

AnimalsAntigen PresentationAnti-Inflammatory Agents, Non-SteroidalAntioxidantsCells, CulturedCurcuminDendritic CellsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease Models, AnimalHumansInterferon-gammaLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred NODAnti-Inflammatory Agents, Non-SteroidalAntioxidantsCurcuminInterferon-gammaNF-kappa BT-bet Transcription FactorT-Box Domain Proteinsdendritic cellsinflammationNOD mouseT-betT lymphocytes

Identifiers

PMID24628444
PMCPMC4089164
OpenAlexW1753833909

What OpenQuestion holds

Textmetadata
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.