Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism

Asthma is a chronic inflammatory disease of the airways characterized by immune cell infiltrates, bronchial hyperresponsiveness, and declining lung function. Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway t...

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Veröffentlicht in:Oxidative medicine and cellular longevity 2020, Vol.2020 (2020), p.1-16
Hauptverfasser: Silva, Alexandre Sérgio, Vieira, Giciane C., Tibério, Iolanda de F. L. C., Madruga, Marta S., Cavalcante, Fabiana de A., da Silva, Bagnólia Araújo, Cardoso, Glêbia A., Queiroga, Fernando R., Righetti, Renato F., de Souza, Iara Leão Luna, Oliveira, Giuliana A. de, Costa, Alana C., da Conceição Correia Silva, Maria, Vasconcelos, Luiz Henrique C., da Silva, Patrícia M.
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container_end_page 16
container_issue 2020
container_start_page 1
container_title Oxidative medicine and cellular longevity
container_volume 2020
creator Silva, Alexandre Sérgio
Vieira, Giciane C.
Tibério, Iolanda de F. L. C.
Madruga, Marta S.
Cavalcante, Fabiana de A.
da Silva, Bagnólia Araújo
Cardoso, Glêbia A.
Queiroga, Fernando R.
Righetti, Renato F.
de Souza, Iara Leão Luna
Oliveira, Giuliana A. de
Costa, Alana C.
da Conceição Correia Silva, Maria
Vasconcelos, Luiz Henrique C.
da Silva, Patrícia M.
description Asthma is a chronic inflammatory disease of the airways characterized by immune cell infiltrates, bronchial hyperresponsiveness, and declining lung function. Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway tissue exhibited peribronchial inflammatory infiltrate, epithelial hyperplasia, and smooth muscle thickening in guinea pigs submitted to ovalbumin sensitization, which were prevented by virgin coconut oil supplementation. Additionally, in animals with lung inflammation, trachea contracted in response to ovalbumin administration, showed a greater contractile response to carbachol (CCh) and histamine, and these responses were prevented by the virgin coconut oil supplementation. Apocynin, a NADPH oxidase inhibitor, did not reduce the potency of CCh, whereas tempol, a superoxide dismutase mimetic, reduced potency only in nonsensitized animals. Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. Therefore, the virgin coconut oil supplementation reverses peribronchial inflammatory infiltrate, epithelial hyperplasia, smooth muscle thickening, and hypercontractility through oxidative stress and its interactions with the NO pathway.
doi_str_mv 10.1155/2020/5148503
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L. C. ; Madruga, Marta S. ; Cavalcante, Fabiana de A. ; da Silva, Bagnólia Araújo ; Cardoso, Glêbia A. ; Queiroga, Fernando R. ; Righetti, Renato F. ; de Souza, Iara Leão Luna ; Oliveira, Giuliana A. de ; Costa, Alana C. ; da Conceição Correia Silva, Maria ; Vasconcelos, Luiz Henrique C. ; da Silva, Patrícia M.</creator><contributor>Moorthy, Bhagavatula ; Bhagavatula Moorthy</contributor><creatorcontrib>Silva, Alexandre Sérgio ; Vieira, Giciane C. ; Tibério, Iolanda de F. L. C. ; Madruga, Marta S. ; Cavalcante, Fabiana de A. ; da Silva, Bagnólia Araújo ; Cardoso, Glêbia A. ; Queiroga, Fernando R. ; Righetti, Renato F. ; de Souza, Iara Leão Luna ; Oliveira, Giuliana A. de ; Costa, Alana C. ; da Conceição Correia Silva, Maria ; Vasconcelos, Luiz Henrique C. ; da Silva, Patrícia M. ; Moorthy, Bhagavatula ; Bhagavatula Moorthy</creatorcontrib><description>Asthma is a chronic inflammatory disease of the airways characterized by immune cell infiltrates, bronchial hyperresponsiveness, and declining lung function. Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway tissue exhibited peribronchial inflammatory infiltrate, epithelial hyperplasia, and smooth muscle thickening in guinea pigs submitted to ovalbumin sensitization, which were prevented by virgin coconut oil supplementation. Additionally, in animals with lung inflammation, trachea contracted in response to ovalbumin administration, showed a greater contractile response to carbachol (CCh) and histamine, and these responses were prevented by the virgin coconut oil supplementation. Apocynin, a NADPH oxidase inhibitor, did not reduce the potency of CCh, whereas tempol, a superoxide dismutase mimetic, reduced potency only in nonsensitized animals. Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. 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Vasconcelos et al.</rights><rights>COPYRIGHT 2020 John Wiley &amp; Sons, Inc.</rights><rights>Copyright © 2020 Luiz Henrique C. Vasconcelos et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Luiz Henrique C. 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Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. 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Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway tissue exhibited peribronchial inflammatory infiltrate, epithelial hyperplasia, and smooth muscle thickening in guinea pigs submitted to ovalbumin sensitization, which were prevented by virgin coconut oil supplementation. Additionally, in animals with lung inflammation, trachea contracted in response to ovalbumin administration, showed a greater contractile response to carbachol (CCh) and histamine, and these responses were prevented by the virgin coconut oil supplementation. Apocynin, a NADPH oxidase inhibitor, did not reduce the potency of CCh, whereas tempol, a superoxide dismutase mimetic, reduced potency only in nonsensitized animals. Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. Therefore, the virgin coconut oil supplementation reverses peribronchial inflammatory infiltrate, epithelial hyperplasia, smooth muscle thickening, and hypercontractility through oxidative stress and its interactions with the NO pathway.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32089769</pmid><doi>10.1155/2020/5148503</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-5462-9459</orcidid><orcidid>https://orcid.org/0000-0003-0161-4891</orcidid><orcidid>https://orcid.org/0000-0001-6926-482X</orcidid><orcidid>https://orcid.org/0000-0001-6234-1458</orcidid><oa>free_for_read</oa></addata></record>
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source PubMed Central Open Access; Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection
subjects Analysis
Animals
Antioxidants
Asthma
Caustic soda
Disease
Ethylenediaminetetraacetic acid
Fatty acids
Food
Histamine
Hyperplasia
Inflammation
Inflammatory diseases
Nitric oxide
Oxidases
Pessoa, João
Phenolphthalein
Potassium
Prevention
Smooth muscle
Sodium
title Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism
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