Evidence map›Paper›PMID 20462420›Full record

ArticleJournal of inflammation (London, England)2010

Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB.

José L Miguel-Carrasco, Sonia Zambrano, Antonio J Blanca, Alfonso Mate, Carmen M Vázquez

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.7field-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

62 citing papers in PubMed, 140 citations in OpenAlex.

  1. Trial
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  5. Cardioprotective Role of Captopril: From Basic to Applied Investigations.International journal of molecular sciences · 2025
    Review
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2 more citing papers are in PubMed but not listed here.

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 1 country.

José L Miguel-CarrascoDepartamento de Fisiología y Zoología, Facultad de Farmacia, Universidad de Sevilla, E-41012 Sevilla, Spain. vazquez@us.es.
Sonia Zambrano
Antonio J Blanca
Alfonso Mate
Carmen M Vázquez
Universidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCaptopril is an angiotensin-converting enzyme (ACE) inhibitor widely used in the treatment of arterial hypertension and cardiovascular diseases. Our objective was to study whether captopril is able to attenuate the cardiac inflammatory process associated with arterial hypertension.

methodsLeft ventricle mRNA expression and plasma levels of pro-inflammatory (interleukin-1beta (IL-1beta) and IL-6) and anti-inflammatory (IL-10) cytokines, were measured in spontaneously hypertensive rats (SHR) and their control normotensive, Wistar-Kyoto (WKY) rats, with or without a 12-week treatment with captopril (80 mg/Kg/day; n = six animals per group). To understand the mechanisms involved in the effect of captopril, mRNA expression of ACE, angiotensin II type I receptor (AT1R) and p22phox (a subunit of NADPH oxidase), as well as NF-kappaB activation and expression, were measured in the left ventricle of these animals.

resultsIn SHR, the observed increases in blood pressures, heart rate, left ventricle relative weight, plasma levels and cardiac mRNA expression of IL-1beta and IL-6, as well as the reductions in the plasma levels and in the cardiac mRNA expression of IL-10, were reversed after the treatment with captopril. Moreover, the mRNA expressions of ACE, AT1R and p22phox, which were enhanced in the left ventricle of SHR, were reduced to normal values after captopril treatment. Finally, SHR presented an elevated cardiac mRNA expression and activation of the transcription nuclear factor, NF-kappaB, accompanied by a reduced expression of its inhibitor, IkappaB; captopril administration corrected the observed changes in all these parameters.

conclusionThese findings show that captopril decreases the inflammation process in the left ventricle of hypertensive rats and suggest that NF-kappaB-driven inflammatory reactivity might be responsible for this effect through an inactivation of NF-kappaB-dependent pro-inflammatory factors.

Identifiers

PMID20462420
PMCPMC2879251
OpenAlexW2142248480

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Registered trials

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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.