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Biapenem as a Novel Insight into Drug Repositioning against Particulate Matter-Induced Lung Injury.
Lee, Wonhwa; Baek, Moon-Chang; Kim, Kyung-Min; Bae, Jong-Sup.
Afiliación
  • Lee W; College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, BK21 Plus KNU Multi-Omics based Creative Drug Research Team, Kyungpook National University, Daegu 41566, Korea.
  • Baek MC; Department of Molecular Medicine, CMRI, School of Medicine, Kyungpook National University, Daegu 41566, Korea.
  • Kim KM; Division of Plant Biosciences, School of Applied BioSciences, College of Agriculture and Life Science, Kyungpook National University, Daegu 41566, Korea.
  • Bae JS; College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, BK21 Plus KNU Multi-Omics based Creative Drug Research Team, Kyungpook National University, Daegu 41566, Korea.
Int J Mol Sci ; 21(4)2020 Feb 21.
Article en En | MEDLINE | ID: mdl-32098061
The screening of biologically active chemical compound libraries can be an efficient way to reposition Food and Drug Adminstration (FDA)-approved drugs or to discover new therapies for human diseases. Particulate matter with an aerodynamic diameter equal to or less than 2.5 µm (PM2.5) is a form of air pollutant that causes significant lung damage when inhaled. This study illustrates drug repositioning with biapenem (BIPM) for the modulation of PM-induced lung injury. Biapenem was used for the treatment of severe infections. Mice were treated with BIPM via tail-vein injection after the intratracheal instillation of PM2.5. Alterations in the lung wet/dry weight, total protein/total cell count and lymphocyte count, inflammatory cytokines in the bronchoalveolar lavage fluid (BALF), vascular permeability, and histology were monitored in the PM2.5-treated mice. BIPM effectively reduced the pathological lung injury, lung wet/dry weight ratio, and hyperpermeability caused by PM2.5. Enhanced myeloperoxidase (MPO) activity by PM2.5 in the pulmonary tissue was inhibited by BIPM. Moreover, increased levels of inflammatory cytokines and total protein by PM2.5 in the BALF were also decreased by BIPM treatment. In addition, BIPM markedly suppressed PM2.5-induced increases in the number of lymphocytes in the BALF. Additionally, the activity of mammalian target of rapamycin (mTOR) was increased by BIPM. Administration of PM2.5 increased the expression levels of toll-like receptor 4 (TLR4), MyD88, and the autophagy-related proteins LC3 II and Beclin 1, which were suppressed by BIPM. In conclusion, these findings indicate that BIPM 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 pulmonary injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tienamicinas / Material Particulado / Lesión Pulmonar / Reposicionamiento de Medicamentos / Pulmón Límite: Animals Idioma: En Revista: Int J Mol Sci Año: 2020 Tipo del documento: Article Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tienamicinas / Material Particulado / Lesión Pulmonar / Reposicionamiento de Medicamentos / Pulmón Límite: Animals Idioma: En Revista: Int J Mol Sci Año: 2020 Tipo del documento: Article Pais de publicación: Suiza