Evidence map›Paper›PMID 24416726›Full record

ArticleJournal of diabetes research2013

Boldine prevents renal alterations in diabetic rats.

Romina Hernández-Salinas, Alejandra Z Vielma, Marlene N Arismendi, Mauricio P Boric, Juan C Sáez, Victoria Velarde

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

36 citing papers in PubMed, 76 citations in OpenAlex.

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  12. Boldine Alters Serum Lipidomic Signatures after Acute Spinal Cord Transection in Male Mice.International journal of environmental research and public health · 2023
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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.

Romina Hernández-SalinasDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
Alejandra Z VielmaDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
Marlene N ArismendiDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
Mauricio P BoricDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
Juan C SáezDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile ; Instituto Milenio, Centro Interdisciplinario de Neurociencias de Valparaíso, Valparaíso, Chile.
Victoria VelardeDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
Pontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy alters both structure and function of the kidney. These alterations are associated with increased levels of reactive oxygen species, matrix proteins, and proinflammatory molecules. Inflammation decreases gap junctional communication and increases hemichannel activity leading to increased membrane permeability and altering tissue homeostasis. Since current treatments for diabetic nephropathy do not prevent renal damage, we postulated an alternative treatment with boldine, an alkaloid obtained from boldo with antioxidant, anti-inflammatory, and hypoglycemic effects. Streptozotocin-induced diabetic and control rats were treated or not treated with boldine (50 mg/Kg/day) for ten weeks. In addition, mesangial cells were cultured under control conditions or in high glucose concentration plus proinflammatory cytokines, with or without boldine (100 µmol/L). Boldine treatment in diabetic animals prevented the increase in glycemia, blood pressure, renal thiobarbituric acid reactive substances and the urinary protein/creatinine ratio. Boldine also reduced alterations in matrix proteins and markers of renal damage. In mesangial cells, boldine prevented the increase in oxidative stress, the decrease in gap junctional communication, and the increase in cell permeability due to connexin hemichannel activity induced by high glucose and proinflammatory cytokines but did not block gap junction channels. Thus boldine prevented both renal and cellular alterations and could be useful for preventing tissue damage in diabetic subjects.

Indexed as

AnimalsAntioxidantsAporphinesCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesDrug Evaluation, PreclinicalKidney Function TestsMalePeumusPlant ExtractsRatsRats, Sprague-DawleyAntioxidantsAporphinesboldinePlant Extracts

Identifiers

PMID24416726
PMCPMC3876708
OpenAlexW2137549051

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.