Evidence map›Paper›PMID 27717985›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2017

Thymoquinone mitigate ischemia-reperfusion-induced liver injury in rats: a pivotal role of nitric oxide signaling pathway.

Mohamed Abd-Elbaset, El-Shaimaa A Arafa, Gamal A El Sherbiny, Mohamed S Abdel-Bakky, Abdel Nasser A M Elgendy

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
10.3field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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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

5 authors at 3 institutions in 2 countries.

Mohamed Abd-ElbasetDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, 62514, Egypt.
El-Shaimaa A ArafaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, 62514, Egypt. elshimaa.arafa@pharm.bsu.edu.eg.
Gamal A El SherbinyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Kafr El-Sheikh University, Kafr El-Sheikh, Egypt.
Mohamed S Abdel-BakkyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt.
Abdel Nasser A M ElgendyDepartment of Pharmacology, Faculty of Veterinary medicine, Beni-Suef University, Beni-Suef, 62514, Egypt.
Beni-Suef University · EGAl Jouf University · SAKafrelsheikh University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative and nitrosative stress-induced endothelial cell damage play an essential role in the pathogenesis of hepatic ischemia-reperfusion (IR) injury. IR is associated with reduced eNOS expression and exacerbated by superimposed stress. NOSTRIN induces intracellular endothelial nitric oxide synthase (eNOS) translocation and inducible nitric oxide synthase (iNOS) increases nitric oxide (NO) production. Our aim was to assess hepatic expression of iNOS, eNOS, and NOSTRIN in IR with or without N-acetylcysteine (NAC) or thymoquinone (TQ) pretreatment and to compare their hepatoprotective effects. Surgical induction of IR was performed by occlusion of hepatic pedicle for 30 min with mini-clamp and reperfused for 30 min. The effects of TQ (20 mg/kg/day) or NAC (300 mg/kg/day) administered orally for 10 days were evaluated by serum ALT and AST, oxidative stress parameters, NO production, and histopathological analysis. Also, localization and expression of iNOS, eNOS, and NOSTRIN were assessed by immunofluorescence. TQ or NAC pretreatment significantly decreased elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and myeloperoxidase (MPO) activities, malondialdehyde (MDA) level, and NO production. In addition, they restored the depleted GSH content and alleviated histopathological changes. Furthermore, they up-regulated eNOS and down-regulated iNOS and NOSTRIN expressions. TQ exerts its hepatoprotective effect, at least in part, by nitric oxide signaling pathway through modulation of iNOS, eNOS, and NOSTRIN expressions as well as suppression of oxidative stress.

Indexed as

AcetylcysteineAlanine TransaminaseAnimalsAntioxidantsAspartate AminotransferasesBenzoquinonesBiomarkersCytoprotectionDisease Models, AnimalGlutathioneLipid PeroxidationLiverLiver DiseasesMaleNitric OxideNitric Oxide Synthase Type IIAcetylcysteineAlanine TransaminaseAntioxidantsAspartate AminotransferasesBenzoquinonesBiomarkersGlutathioneNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, ratNos3 protein, ratPeroxidasethymoquinoneeNOSHepatic ischemia–reperfusioniNOSNOSTRINThymoquinone

Identifiers

PMID27717985
OpenAlexW2528986219

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.