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Nutrients 2018, 10(3), 263; https://doi.org/10.3390/nu10030263

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

1
Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE
2
Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE
3
Department of Pharmacology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666 Al Ain, UAE
4
Department of Pharmacology and Clinical Pharmacy, College of Medicine & Health Sciences, Sultan Qaboos University, P.O. Box 35, Muscat 123, Al-Khod, Oman
*
Author to whom correspondence should be addressed.
Received: 2 January 2018 / Revised: 18 January 2018 / Accepted: 23 January 2018 / Published: 26 February 2018
(This article belongs to the Special Issue Antioxidants in Health and Disease)
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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. View Full-Text
Keywords: diesel exhaust particles; nootkatone; airway resistance; Lung; oxidative stress; inflammation; NF-κB diesel exhaust particles; nootkatone; airway resistance; Lung; oxidative stress; inflammation; NF-κB
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Nemmar, A.; Al-Salam, S.; Beegam, S.; Yuvaraju, P.; Hamadi, N.; Ali, B.H. In Vivo Protective Effects of Nootkatone against Particles-Induced Lung Injury Caused by Diesel Exhaust Is Mediated via the NF-κB Pathway. Nutrients 2018, 10, 263.

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