Evidence map›Paper›PMID 26221999›Full record

ArticleRedox report : communications in free radical research2016

Nigella sativa oil attenuates chronic nephrotoxicity induced by oral sodium nitrite: Effects on tissue fibrosis and apoptosis.

Mohammed M H Al-Gayyar, Hanan M Hassan, Abdullah Alyoussef, Ahmed Abbas, Mohamed M Darweish, Amany A El-Hawwary

Open access · bronzeAbstract read
In one paragraph

Article in Redox report : communications in free radical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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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 3 institutions in 2 countries.

Mohammed M H Al-Gayyara Department of Pharmaceutical Chemistry, Faculty of Pharmacy , University of Tabuk , Saudi Arabia.
Hanan M Hassanc Department of Pharmaceutical Sciences, College of Pharmacy , Princess Noura bint Abulrahman University , Riyadh 11671 , KSA.
Abdullah Alyoussefd Department of Internal Medicine, Faculty of Medicine , University of Tabuk , Saudi Arabia.
Ahmed Abbase Department of Pharmacognosy, Faculty of Pharmacy , University of Mansoura , Egypt.
Mohamed M Darweisha Department of Pharmaceutical Chemistry, Faculty of Pharmacy , University of Tabuk , Saudi Arabia.
Amany A El-Hawwaryf Department of Histology and Cell Biology, Faculty of Medicine , University of Mansoura , Egypt.
Mansoura University · EGUniversity of Tabuk · SADelta University for Science and Technology · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSodium nitrite, a food preservative, has been reported to increase oxidative stress indicators such as lipid peroxidation, which can affect different organs including the kidney. Here, we investigated the toxic effects of oral sodium nitrite on kidney function in rats and evaluated potential protective effects of Nigella sativa oil (NSO).

methodsSeventy adult male Sprague-Dawley rats received 80 mg/kg sodium nitrite orally in the presence or absence of NSO (2.5, 5, and 10 ml/kg) for 12 weeks. Morphological changes were assessed by hematoxylin and eosin, Mallory trichome, and periodic acid-Schiff staining. Renal tissues were used for measurements of oxidative stress markers, C-reactive protein, cytochrome C oxidase, transforming growth factor (TGF)-beta1, monocyte chemotactic protein (MCP)-1, pJNK/JNK, and caspase-3.

resultsNSO significantly reduced sodium nitrite-induced elevation in serum urea and creatinine, as well as increasing normal appearance of renal tissue. NSO also prevented reductions in glycogen levels caused by sodium nitrite alone. Moreover, NSO treatment resulted in dose-dependent significant reductions in fibrosis markers after sodium nitrite-induced 3- and 2.7-fold increase in MCP-1 and TGF-beta1, respectively. Finally, NSO partially reduced the elevated caspase-3 and pJNK/JNK. DISCUSSION: NSO ameliorates sodium nitrite-induced nephrotoxicity through blocking oxidative stress, attenuation of fibrosis/inflammation, restoration of glycogen level, amelioration of cytochrome C oxidase, and inhibition of apoptosis.

Indexed as

AnimalsAntioxidantsApoptosisCarumCaspase 3Chemokine CCL2C-Reactive ProteinCreatinineFibrosisKidneyLipid PeroxidationLiverMaleNigella sativaOxidative StressPlant OilsAntioxidantscaraway oilCaspase 3Chemokine CCL2C-Reactive ProteinCreatininePlant OilsSodium NitriteTransforming Growth Factor beta1UreaBlack cuminCRPCytochrome C oxidaseGlycogenMCP-1TGF-beta1

Identifiers

PMID26221999
PMCPMC6837667
OpenAlexW1503743739

What OpenQuestion holds

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Read underepoch 390

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.