Evidence map›Paper›PMID 26670366›Full record

ArticleJournal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques2015

In vitro Treatment with cis-[Ru(H-dcbpy-)2(Cl)(NO)] Improves the Endothelial Function in Aortic Rings with Endothelial Dysfunction.

Jorge Camargo Oishi, Tereza Cristina Buzinnari, Cezar Rangel Pestana, Thiago Francisco De Moraes, Izabela Pereira Vatanabe, David Anderson Wink, Roberto Santana da Silva, Lusiane Maria Bendhack, Gerson Jhonatan Rodrigues

Open access · diamondAbstract read
In one paragraph

Article in Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Cardioprotective effects of a ruthenium (II) Schiff base complex in diet-induced prediabetic rats.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Article
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 1 institution in 1 country.

Jorge Camargo OishiDepartamento de Ciências Fisiológicas, Universidade Federal de São Carlos, Brazil...
Tereza Cristina Buzinnari
Cezar Rangel Pestana
Thiago Francisco De Moraes
Izabela Pereira Vatanabe
David Anderson Wink
Roberto Santana da Silva
Lusiane Maria Bendhack
Gerson Jhonatan Rodrigues
Universidade Federal de São Carlos · BR

Funding

NITRIC OXIDE AS A MODIFIER OF OXIDATIVE STRESSZ01SC007281 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID A · 1996 to 2008
$1.8M
Redox Mechanism Process of Angiogenesis and Wound HealingZ01BC010898 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2008 to 2008
$436k
Intramural NIH HHS Z01 BC010898Intramural NIH HHS Z01 SC007281
6 · The paper itself

Abstract

purposeThe ruthenium complex cis-[Ru(H-dcbpy-)2(Cl)(NO)] (DCBPY) is a nitric oxide (NO) donor and studies suggested that the ruthenium compounds can inactivate O2-. The aim of this study is to test if DCBPY can revert and/or prevent the endothelial dysfunction.

methodsNormotensive (2K) and hypertensive (2K-1C) wistar rats were used. To vascular reactivity study, thoracic aortas were isolated, rings with intact endothelium were incubated with: DCBPY: 0.1; 1 and 10μM, DCBPY plus hydroxocobalin (NO scavenger) or tempol during 30 minutes, and concentration effect curves to acetylcholine were performed. The potency values (pD2) and maximum effect (ME) were analyzed. The O2- was generated using hypoxantine xantine oxidase and the reduction of cytochrome c, NO consumption by O2- and the effect in avoid NO consumption was measured.

resultsIn 2K-1C DCBPY at 0.1; 1 or 10μM improved the relaxation endothelium dependent induced by acetylcholine in aortic rings compared to control 2K-1C, and also improved ME. In rings from 2K incubation with DCBPY (0.1; 1.0 and 10 μM) did not change pD2 or ME. Incubation with 0.1 μM of DCBPY plus hydroxocobalamin did not modify the potency and ME in 2K-1C compared to DCBPY (0.1 μM). DCBPY and SOD inhibits the reduction of cytochrome c and inhibited the NO consumption by O2-, showing that O2- has been removed from the solution.

conclusionOur results suggest that DCBPY at a lower concentration (0.1 µM) is not an NO generator, but can inactivate superoxide and improves the endothelial function.

Indexed as

AcetylcholineAnimalsAntioxidantsAorta, ThoracicCoordination ComplexesEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsIn Vitro TechniquesMaleMuscle RelaxationNitric OxideOxygen ConsumptionRatsRats, WistarVascular DiseasesAcetylcholineAntioxidantsCoordination ComplexesNitric OxideVasodilator Agents

Identifiers

PMID26670366
PMCPMC8335899
OpenAlexW2173140528

What OpenQuestion holds

Textmetadata
LicenceTDM
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.