EC-18, a synthetic monoacetyldiglyceride (1-palmitoyl-2-linoleoyl-3- acetylglycerol), attenuates the asthmatic response in an aluminum hydroxide/ovalbumin-induced model of asthma

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dc.contributor.authorIn Sik Shin-
dc.contributor.authorNa Rae Shin-
dc.contributor.authorChan Mi Jeon-
dc.contributor.authorOk-Kyoung Kwon-
dc.contributor.authorK Y Sohn-
dc.contributor.authorT S Lee-
dc.contributor.authorJae Wha Kim-
dc.contributor.authorKyung Seop Ahn-
dc.contributor.authorSei-Ryang Oh-
dc.date.accessioned2017-04-19T09:49:26Z-
dc.date.available2017-04-19T09:49:26Z-
dc.date.issued2014-
dc.identifier.issn15675769-
dc.identifier.uri10.1016/j.intimp.2013.11.006ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11749-
dc.description.abstractEC-18 is a synthetic monoacetyldiaglyceride that is a major constituent in antlers of Sika deer (Cervus nippon Temmenick). In this study, we evaluated the protective effects of EC-18 on Th2-type cytokines, eosinophil infiltration, and other factors in an aluminum hydroxide/ovalbumin (OVA)-induced murine asthma model. Mice were sensitized on days 0 and 14 by intraperitoneal injection of OVA with aluminum hydroxide. On days 21, 22 and 23 after the initial sensitization, the mice received an airway challenge with OVA for 1 h using an ultrasonic nebulizer. EC-18 was administered to mice by oral gavage at doses of 30 mg/kg and 60 mg/kg once daily from day 18 to 23. Methacholine responsiveness was measured 24 h after the final OVA challenge, and the bronchoalveolar lavage fluid (BALF) was collected 48 h after the final OVA challenge. EC-18 significantly reduced methacholine responsiveness, T helper type 2 (Th2) cytokines, eotaxin-1, immunoglobulin (Ig) E, IgG, and the number of inflammatory cells. In addition, EC-18-treated mice exhibited the reduction in the expression of inducible nitric oxide synthase (iNOS) in lung tissue. In the histological analysis using hematoxylin-eosin stain and periodic acid-Schiff stain, EC-18 attenuated the infiltration of inflammatory cells into the airway and reduced the level of mucus production. Our results showed that EC-18 effectively suppressed the asthmatic response induced by OVA challenge. These effects were considered to be associated with iNOS suppression. In conclusion, this study suggests that EC-18 may be a therapeutic agent for allergic asthma-
dc.publisherElsevier-
dc.titleEC-18, a synthetic monoacetyldiglyceride (1-palmitoyl-2-linoleoyl-3- acetylglycerol), attenuates the asthmatic response in an aluminum hydroxide/ovalbumin-induced model of asthma-
dc.title.alternativeEC-18, a synthetic monoacetyldiglyceride (1-palmitoyl-2-linoleoyl-3- acetylglycerol), attenuates the asthmatic response in an aluminum hydroxide/ovalbumin-induced model of asthma-
dc.typeArticle-
dc.citation.titleInternational Immunopharmacology-
dc.citation.number1-
dc.citation.endPage123-
dc.citation.startPage116-
dc.citation.volume18-
dc.contributor.affiliatedAuthorOk-Kyoung Kwon-
dc.contributor.affiliatedAuthorJae Wha Kim-
dc.contributor.affiliatedAuthorKyung Seop Ahn-
dc.contributor.affiliatedAuthorSei-Ryang Oh-
dc.contributor.alternativeName신인식-
dc.contributor.alternativeName신나래-
dc.contributor.alternativeName전찬미-
dc.contributor.alternativeName권옥경-
dc.contributor.alternativeName손기영-
dc.contributor.alternativeName이태숙-
dc.contributor.alternativeName김재화-
dc.contributor.alternativeName안경섭-
dc.contributor.alternativeName오세량-
dc.identifier.bibliographicCitationInternational Immunopharmacology, vol. 18, no. 1, pp. 116-123-
dc.identifier.doi10.1016/j.intimp.2013.11.006-
dc.subject.keywordAsthma-
dc.subject.keywordCytokines-
dc.subject.keywordEC-18-
dc.subject.keywordInducible nitric oxide synthase-
dc.subject.keywordMonoacetyldiacylglyceride-
dc.subject.localAsthma-
dc.subject.localCytokines-
dc.subject.localCytokine-
dc.subject.localEC-18-
dc.subject.localInducible nitric oxide synthase-
dc.subject.localInducible nitric oxide synthase (iNOS)-
dc.subject.localMonoacetyldiacylglyceride-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
Division of Biomaterials Research > Cell Factory Research Center > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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