Evidence map›Paper›PMID 23804455›Full record

ArticleAmerican journal of physiology. Renal physiology2013

The antioxidant silybin prevents high glucose-induced oxidative stress and podocyte injury in vitro and in vivo.

Khaled Khazim, Yves Gorin, Rita Cassia Cavaglieri, Hanna E Abboud, Paolo Fanti

Registry-linked trialAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01265563 (Correction of Glutathione Deficiency for Treatment of Diabetic Nephropathy), which is not on this map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
7.6field-weighted citation impact, top 2% 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.

NCT01265563 phase2completednot on this map

Correction of Glutathione Deficiency for Treatment of Diabetic Nephropathy

TypeinterventionalSponsorVA Office of Research and DevelopmentRan2011 to 2016Enrolled108ConditionsDiabetic Nephropathy, Proteinuria, Oxidative StressArmsN-acetylcysteine placebo and silibin placebo, N-acetylcysteine active and silibin placebo, N-acetylcysteine placebo and silibin active, N-acetylcysteine active and silibin active, N-acetylcysteine active + high-dose silibin active
3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  9. Review
  10. Nutrients · 2023
    Review
  11. The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
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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

5 authors at 1 institution in 2 countries.

Khaled KhazimUniv. of Texas Health Science Center, Dept. of Medicine, Division of Nephrology MC 7882, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Yves Gorin
Rita Cassia Cavaglieri
Hanna E Abboud
Paolo Fanti
The University of Texas Health Science Center at San Antonio · US

Funding

Mechanism of eNOS Uncoupling in the Renal MicrovasculatureR01DK079996 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GORIN, YVES CLAUDE · 2010 to 2014
$1.5M
Tubular epithelial cell injuryR01DK033665 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GORIN, YVES CLAUDE · 1986 to 2015
$1.3M
NIDDK NIH HHS R01 DK033665NIDDK NIH HHS R01 DK 079996NIDDK NIH HHS R01 DK079996
6 · The paper itself

Abstract

Podocyte injury, a major contributor to the pathogenesis of diabetic nephropathy, is caused at least in part by the excessive generation of reactive oxygen species (ROS). Overproduction of superoxide by the NADPH oxidase isoform Nox4 plays an important role in podocyte injury. The plant extract silymarin is attributed antioxidant and antiproteinuric effects in humans and in animal models of diabetic nephropathy. We investigated the effect of silybin, the active constituent of silymarin, in cultures of mouse podocytes and in the OVE26 mouse, a model of type 1 diabetes mellitus and diabetic nephropathy. Exposure of podocytes to high glucose (HG) increased 60% the intracellular superoxide production, 90% the NADPH oxidase activity, 100% the Nox4 expression, and 150% the number of apoptotic cells, effects that were completely blocked by 10 μM silybin. These in vitro observations were confirmed by similar in vivo findings. The kidney cortex of vehicle-treated control OVE26 mice displayed greater Nox4 expression and twice as much superoxide production than cortex of silybin-treated mice. The glomeruli of control OVE26 mice displayed 35% podocyte drop out that was not present in the silybin-treated mice. Finally, the OVE26 mice experienced 54% more pronounced albuminuria than the silybin-treated animals. In conclusion, this study demonstrates a protective effect of silybin against HG-induced podocyte injury and extends this finding to an animal model of diabetic nephropathy.

Indexed as

AnimalsAntioxidantsDiabetes Mellitus, Type 1Diabetic NephropathiesDisease Models, AnimalGlucoseMiceNADPH Oxidase 4NADPH OxidasesOxidative StressPodocytesReactive Oxygen SpeciesSilybinSilymarinSuperoxidesAntioxidantsGlucoseNADPH Oxidase 4NADPH OxidasesNox4 protein, mouseReactive Oxygen SpeciesSilybinSilymarinSuperoxidesalbuminuriaapoptosisdiabetic nephropathyNADPH oxidasephytochemicals

Identifiers

PMID23804455
PMCPMC3761209
OpenAlexW2095703659

What OpenQuestion holds

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Registered trials

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.