Evidence map›Paper›PMID 26199914›Full record

ArticleCell journal2015

N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation.

Sobia Mushtaq, Tahir Ali, Qamar Javed, Sobia Tabassum, Iram Murtaza

Abstract read
In one paragraph

Article in Cell journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

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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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Melatonin abated Bisphenol A-induced neurotoxicity via p53/PUMA/Drp-1 signaling.Environmental science and pollution research international · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. 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

5 authors.

Sobia MushtaqDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, 45320, Pakistan.
Tahir AliDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, 45320, Pakistan.
Qamar JavedDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, 45320, Pakistan.
Sobia TabassumDepartment of Biotechnology, International Islamic University, Islamabad, Pakistan.
Iram MurtazaDepartment of Biochemistry, Quaid-i-Azam University, Islamabad, 45320, Pakistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOxidative stress down regulates antioxidant enzymes including superoxide dismutase (SOD) and contributes to the development of cardiac hypertrophy. N-Acetyl cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the inhibitory role of NAC against endothelin-1 (ET-1)-induced cardiac hypertrophy. MATERIALS AND

methodsIn this experimental study at QAU from January, 2013 to March, 2013. ET-1 (50 µg/kg) and NAC (50 mg/kg) were given intraperitoneally to 6-day old neonatal rats in combination or alone. All rats were sacrificed 15 days after the final injection. Histological analysis was carried out to observe the effects caused by both drugs. Reactive oxygen species (ROS) analysis and SOD assay were also carried out. Expression level of hyper- trophic marker, brain natriuretic peptide (BNP), was detected by western blotting.

resultsOur findings showed that ET-1-induced cardiac hypertrophy leading towards heart failure was due to the imbalance of different parameters including free radical-induced oxidative stress and antioxidative enzymes such as SOD. Furthermore NAC acted as an antioxidant and played inhibitory role against ROS-dependent hypertrophy via regulatory role of SOD as a result of oxidative response associated with hypertrophy.

conclusionET-1-induced hypertrophic response is associated with increased ROS production and decreased SOD level, while NAC plays a role against free radicals-induced oxidative stress via SOD regulation.

Indexed as

Cardiac HypertrophyEndothelin-1Oxidative StressReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID26199914
PMCPMC4503849

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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.