Evidence map›Paper›PMID 29495362›Full record

ArticleNutrients2018

In Vivo Protective Effects of Nootkatone against Particles-Induced Lung Injury Caused by Diesel Exhaust Is Mediated via the NF-κB Pathway.

Abderrahim Nemmar, Suhail Al-Salam, Sumaya Beegam, Priya Yuvaraju, Naserddine Hamadi, Badreldin H Ali

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 68 citations in OpenAlex.

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  16. Advances on (+)-nootkatone microbial biosynthesis and its related enzymes.Journal of industrial microbiology & biotechnology · 2021
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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 2 institutions in 2 countries.

Abderrahim NemmarDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE. anemmar@uaeu.ac.ae.
Suhail Al-SalamDepartment of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE. suhaila@uaeu.ac.ae.
Sumaya BeegamDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE. sumayab@uaeu.ac.ae.
Priya YuvarajuDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE. priyay@uaeu.ac.ae.
Naserddine HamadiDepartment of Pharmacology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE. hamadinasro@uaeu.ac.ae.
Badreldin H AliDepartment of Pharmacology and Clinical Pharmacy, College of Medicine & Health Sciences, Sultan Qaboos University, P.O. Box 35, Muscat 123, Al-Khod, Oman. alibadreldin@hotmail.com.
United Arab Emirates University · AESultan Qaboos University · OM

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have shown that acute particulate air pollution exposure is linked with pulmonary adverse effects, including alterations of pulmonary function, inflammation, and oxidative stress. Nootkatone, a constituent of grapefruit, has antioxidant and anti-inflammatory effects. However, the effect of nootkatone on lung toxicity has not been reported so far. In this study we evaluated the possible protective effects of nootkatone on diesel exhaust particles (DEP)-induced lung toxicity, and the possible mechanisms underlying these effects. Mice were intratracheally (i.t.) instilled with either DEP (30 µg/mouse) or saline (control). Nootkatone was given to mice by gavage, 1 h before i.t. instillation, with either DEP or saline. Twenty-four hours following DEP exposure, several physiological and biochemical endpoints were assessed. Nootkatone pretreatment significantly prevented the DEP-induced increase in airway resistance in vivo, decreased neutrophil infiltration in bronchoalveolar lavage fluid, and abated macrophage and neutrophil infiltration in the lung interstitium, assessed by histolopathology. Moreover, DEP caused a significant increase in lung concentrations of 8-isoprostane and tumor necrosis factor α, and decreased the reduced glutathione concentration and total nitric oxide activity. These actions were all significantly alleviated by nootkatone pretreatment. Similarly, nootkatone prevented DEP-induced DNA damage and prevented the proteolytic cleavage of caspase-3. Moreover, nootkatone inhibited nuclear factor-kappaB (NF-κB) induced by DEP. We conclude that nootkatone prevented the DEP-induced increase in airway resistance, lung inflammation, oxidative stress, and the subsequent DNA damage and apoptosis through a mechanism involving inhibition of NF-κB activation. Nootkatone could possibly be considered a beneficial protective agent against air pollution-induced respiratory adverse effects.

Indexed as

AnimalsAnti-Inflammatory AgentsAntioxidantsApoptosisBronchoalveolar Lavage FluidCaspase 3Citrus paradisiComet AssayDinoprostDNA DamageGlutathioneLungLung InjuryMiceMice, Inbred BALB CNeutrophil Infiltration8-epi-prostaglandin F2alphaAnti-Inflammatory AgentsAntioxidantsCasp3 protein, mouseCaspase 3DinoprostGlutathioneNF-kappa BNitric OxidenootkatoneParticulate MatterPolycyclic SesquiterpenesProtective AgentsSesquiterpenesTumor Necrosis Factor-alphaVehicle Emissionsairway resistancediesel exhaust particlesinflammationLungNF-κBnootkatoneoxidative stress

Identifiers

PMID29495362
PMCPMC5872681
OpenAlexW2789942309

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.