Inhibitory functions of maslinic acid on particulate matter-induced lung injury through TLR4-mTOR-autophagy pathways
DC Field | Value | Language |
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dc.contributor.author | Jeong S.Y. | - |
dc.contributor.author | Kim J. | - |
dc.contributor.author | Park E.K. | - |
dc.contributor.author | Baek M.-C. | - |
dc.contributor.author | Bae J.-S. | - |
dc.date.available | 2020-03-03T06:47:01Z | - |
dc.date.created | 2020-02-24 | - |
dc.date.issued | 2020-04 | - |
dc.identifier.issn | 0013-9351 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/17800 | - |
dc.description.abstract | Particulate matter (PM), the collection of all liquid and solid particles suspended in air, includes both organic and inorganic particles, many of which are health-hazards. PM particles with a diameter equal to or less than 2.5 μm (PM2.5) is a form of air pollutant that causes significant lung damage when inhaled. Maslinic acid (MA) prevents oxidative stress and pro-inflammatory cytokine generation, but there is little information available regarding its role in PM-induced lung injury. Therefore, the purpose of this study was to determine the protective activity of MA against PM2.5-induced lung injury. The mice were divided into seven groups (n = 10 each): a mock control group, an MA control (0.8 mg/kg mouse body weight) group, an opted PM2.5 produced from diesel (10 mg/kg mouse body weight) group, a diesel PM2.5+MA (0.2, 0.4, 0.6, and 0.8 mg/kg mouse body weight) groups. Mice were treated with MA via tail-vein injection 30 min after the intratracheal instillation of a diesel PM2.5. Changes in the wet/dry weight ratio of the lung tissue, total protein/total cell and lymphocyte counts, inflammatory cytokines in the bronchoalveolar lavage fluid (BALF), vascular permeability, and histology were monitored in diesel PM2.5-treated mice. The results showed that MA reduced pathological lung injury, the wet/dry weight ratio of the lung tissue, and hyperpermeability caused by diesel PM2.5. MA also inhibited diesel PM2.5-induced myeloperoxidase (MPO) activity in the lung tissue, decreased the levels of diesel PM2.5-induced inflammatory cytokines, including tumor necrosis factor (TNF)-α and interleukin (IL)-1β, reduced nitric oxide (NO) and total protein in the BALF, and effectively attenuated diesel PM2.5-induced increases in the number of lymphocytes in the BALF. In addition, MA increased the protein phosphorylation of the mammalian target of rapamycin (mTOR) and dramatically suppressed diesel PM2.5-stimulated expression of toll-like receptor 4 (TLR4), MyD88, and the autophagy-related proteins LC3 II and Beclin 1. In conclusion, these findings indicate that MA has a critical anti-inflammatory effect due to its ability to regulate both the TLR4-MyD88 and mTOR-autophagy pathways and may thus be a potential therapeutic agent against diesel PM2.5-induced lung injury. © 2020 Elsevier Inc. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | Academic Press Inc. | - |
dc.relation.isPartOf | Environmental Research | - |
dc.title | Inhibitory functions of maslinic acid on particulate matter-induced lung injury through TLR4-mTOR-autophagy pathways | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000526177500052 | - |
dc.identifier.doi | 10.1016/j.envres.2020.109230 | - |
dc.identifier.bibliographicCitation | Environmental Research, v.183 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85079041005 | - |
dc.citation.title | Environmental Research | - |
dc.citation.volume | 183 | - |
dc.contributor.affiliatedAuthor | Kim J. | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Lung injury | - |
dc.subject.keywordAuthor | Maslinic acid | - |
dc.subject.keywordAuthor | Particulate matter | - |
dc.subject.keywordAuthor | TLR4-mTOR-autophagy | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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