Evidence map›Paper›PMID 23347386›Full record

ArticleImmunology2013

Curcumin alleviates immune-complex-mediated glomerulonephritis in factor-H-deficient mice.

Alexander Jacob, Lee Chaves, Michael T Eadon, Anthony Chang, Richard J Quigg, Jessy J Alexander

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Alexander JacobDepartment of Medicine, The University of Chicago, Chicago, IL, USA.
Lee Chaves
Michael T Eadon
Anthony Chang
Richard J Quigg
Jessy J Alexander
University of Chicago · US

Funding

CLINICAL THERAPEUTICST32GM007019 · NIGMS · UNIVERSITY OF CHICAGO · PI Peter Hugh O'Donnell, MARK J RATAIN · 1985 to 2026
$8.7M
Role of the Complement System in Renal DiseaseR01DK041873 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QUIGG, RICHARD J. · 1994 to 2011
$3.4M
PATHOGENIC ROLE OF THE COMPLEMENT SYSTEM IN MURINE LUPUSR01DK055357 · NIDDK · UNIVERSITY OF CHICAGO · PI QUIGG, RICHARD J. · 1999 to 2009
$2.5M
Role of the complement system in renal diseaseR56DK041873 · NIDDK · UNIVERSITY OF CHICAGO · PI QUIGG, RICHARD J · 2006 to 2006
$75k
COMPLEMENT ACTIVATION OF THE GLOMERULER EPITHELIAL CELLR29DK041873 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QUIGG, RICHARD J · 1989 to 1993
–
NIDDK NIH HHS DK041873NIDDK NIH HHS DK055357NIDDK NIH HHS R01 DK041873NIDDK NIH HHS R01 DK055357NIDDK NIH HHS R56 DK041873NIGMS NIH HHS T32 GM007019NIGMS NIH HHS T32GM007019
6 · The paper itself

Abstract

Complement factor H (Cfh) is a key regulator of the complement cascade and protects C57BL/6 mice from immune complex-mediated complement-dependent glomerulonephritis. In chronic serum sickness (CSS) there are increased deposits of immune complexes in the glomeruli with inflammation and a scarring phenotype. As cucurmin is an effective anti-inflammatory agent and reduces complement activation, we hypothesized that it should alleviate renal disease in this setting. To determine the effectiveness of curcumin, an apoferritin-induced CSS model in Cfh-deficient (Cfh(-/-)) mice was used. Curcumin treatment (30 mg/kg) given every day in parallel with apoferritin reduced glomerulonephritis and enhanced kidney function (blood urea nitrogen, 45·4 ± 7·5 versus 35·6 ± 5·1; albuminuria, 50·1 ± 7·1 versus 15·7 ± 7·1; glomerulonephritis, 2·62 + 0·25 versus 2 + 0·3, P < 0·05). In line with reduced IgG deposits in mice with CSS given curcumin, C9 deposits were reduced indicating reduced complement activation. Mice treated with curcumin had a significant reduction in the number of splenic CD19(+) B cells and the ratio of CD19 : CD3 cells (P < 0·05) with no change in the T-cell population. Myeloperoxidase assay showed reduced macrophages in the kidney. However, a significant reduction in the M2 subset of splenic macrophages by apoferritin was prevented by curcumin, suggesting a protective function. Curcumin treatment reduced mRNA expression of inflammatory proteins monocyte chemoattractant protein-1 and transforming growth factor-β and matrix proteins, fibronectin, laminin and collagen. Our results clearly illustrate that curcumin reduces glomerulosclerosis, improves kidney function and could serve as a therapeutic agent during serum sickness.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalApoferritinsChronic DiseaseComplement ActivationComplement Factor HCurcuminGlomerulonephritisHumansImmune Complex DiseasesKidney Function TestsMaleMiceMice, Inbred C57BLSerum SicknessTreatment OutcomeAnti-Inflammatory Agents, Non-SteroidalApoferritinsComplement Factor HCurcumin

Identifiers

PMID23347386
PMCPMC3701179
OpenAlexW2007832071

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.