PlantImRecepV1, Main, Exploration, bibRecord, 000204

Biapenem as a Novel Insight into Drug Repositioning against Particulate Matter-Induced Lung Injury.

Identifieur interne : 000204 ( Main/Exploration ); précédent : 000203; suivant : 000205

Biapenem as a Novel Insight into Drug Repositioning against Particulate Matter-Induced Lung Injury.

Auteurs : Wonhwa Lee [Corée du Sud] ; Moon-Chang Baek [Corée du Sud] ; Kyung-Min Kim [Corée du Sud] ; Jong-Sup Bae [Corée du Sud]

Source :

International journal of molecular sciences [ 1422-0067 ] ; 2020.

RBID : pubmed:32098061

Descripteurs français

KwdFr :
- Animaux (MeSH), Bécline-1 (immunologie), Cytokines (immunologie), Facteur de différenciation myéloïde-88 (immunologie), Lavage bronchoalvéolaire (MeSH), Lymphocytes (immunologie), Lésion pulmonaire (anatomopathologie), Lésion pulmonaire (immunologie), Lésion pulmonaire (induit chimiquement), Lésion pulmonaire (traitement médicamenteux), Matière particulaire (toxicité), Mâle (MeSH), Poumon (anatomopathologie), Poumon (immunologie), Protéines associées aux microtubules (immunologie), Repositionnement des médicaments (MeSH), Récepteur de type Toll-4 (immunologie), Souris (MeSH), Souris de lignée BALB C (MeSH), Sérine-thréonine kinases TOR (immunologie), Thiénamycine (pharmacologie).
MESH :
- anatomopathologie : Lésion pulmonaire, Poumon.
- immunologie : Bécline-1, Cytokines, Facteur de différenciation myéloïde-88, Lymphocytes, Lésion pulmonaire, Poumon, Protéines associées aux microtubules, Récepteur de type Toll-4, Sérine-thréonine kinases TOR.
- induit chimiquement : Lésion pulmonaire.
- pharmacologie : Thiénamycine.
- toxicité : Matière particulaire.
- traitement médicamenteux : Lésion pulmonaire.
- Animaux, Lavage bronchoalvéolaire, Mâle, Repositionnement des médicaments, Souris, Souris de lignée BALB C.

English descriptors

KwdEn :
- Animals (MeSH), Beclin-1 (immunology), Bronchoalveolar Lavage (MeSH), Cytokines (immunology), Drug Repositioning (MeSH), Lung (immunology), Lung (pathology), Lung Injury (chemically induced), Lung Injury (drug therapy), Lung Injury (immunology), Lung Injury (pathology), Lymphocytes (immunology), Male (MeSH), Mice (MeSH), Mice, Inbred BALB C (MeSH), Microtubule-Associated Proteins (immunology), Myeloid Differentiation Factor 88 (immunology), Particulate Matter (toxicity), TOR Serine-Threonine Kinases (immunology), Thienamycins (pharmacology), Toll-Like Receptor 4 (immunology).
MESH :
- chemical , immunology : Beclin-1, Cytokines, Microtubule-Associated Proteins, Myeloid Differentiation Factor 88, TOR Serine-Threonine Kinases, Toll-Like Receptor 4.
- chemically induced : Lung Injury.
- drug therapy : Lung Injury.
- immunology : Lung, Lung Injury, Lymphocytes.
- pathology : Lung, Lung Injury.
- chemical , pharmacology : Thienamycins.
- chemical , toxicity : Particulate Matter.
- Animals, Bronchoalveolar Lavage, Drug Repositioning, Male, Mice, Mice, Inbred BALB C.

Abstract

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 (PM_2.5) 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 PM_2.5. 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 PM_2.5-treated mice. BIPM effectively reduced the pathological lung injury, lung wet/dry weight ratio, and hyperpermeability caused by PM_2.5. Enhanced myeloperoxidase (MPO) activity by PM_2.5 in the pulmonary tissue was inhibited by BIPM. Moreover, increased levels of inflammatory cytokines and total protein by PM_2.5 in the BALF were also decreased by BIPM treatment. In addition, BIPM markedly suppressed PM_2.5-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 PM_2.5 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 PM_2.5-induced pulmonary injury.

DOI: 10.3390/ijms21041462
PubMed: 32098061
PubMed Central: PMC7073049

Affiliations:

Corée du Sud

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000205
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Le document en format XML

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<term>Beclin-1 (immunology)</term>
<term>Bronchoalveolar Lavage (MeSH)</term>
<term>Cytokines (immunology)</term>
<term>Drug Repositioning (MeSH)</term>
<term>Lung (immunology)</term>
<term>Lung (pathology)</term>
<term>Lung Injury (chemically induced)</term>
<term>Lung Injury (drug therapy)</term>
<term>Lung Injury (immunology)</term>
<term>Lung Injury (pathology)</term>
<term>Lymphocytes (immunology)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Microtubule-Associated Proteins (immunology)</term>
<term>Myeloid Differentiation Factor 88 (immunology)</term>
<term>Particulate Matter (toxicity)</term>
<term>TOR Serine-Threonine Kinases (immunology)</term>
<term>Thienamycins (pharmacology)</term>
<term>Toll-Like Receptor 4 (immunology)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Bécline-1 (immunologie)</term>
<term>Cytokines (immunologie)</term>
<term>Facteur de différenciation myéloïde-88 (immunologie)</term>
<term>Lavage bronchoalvéolaire (MeSH)</term>
<term>Lymphocytes (immunologie)</term>
<term>Lésion pulmonaire (anatomopathologie)</term>
<term>Lésion pulmonaire (immunologie)</term>
<term>Lésion pulmonaire (induit chimiquement)</term>
<term>Lésion pulmonaire (traitement médicamenteux)</term>
<term>Matière particulaire (toxicité)</term>
<term>Mâle (MeSH)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<term>Protéines associées aux microtubules (immunologie)</term>
<term>Repositionnement des médicaments (MeSH)</term>
<term>Récepteur de type Toll-4 (immunologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée BALB C (MeSH)</term>
<term>Sérine-thréonine kinases TOR (immunologie)</term>
<term>Thiénamycine (pharmacologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Beclin-1</term>
<term>Cytokines</term>
<term>Microtubule-Associated Proteins</term>
<term>Myeloid Differentiation Factor 88</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Toll-Like Receptor 4</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Lésion pulmonaire</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Lung Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Bécline-1</term>
<term>Cytokines</term>
<term>Facteur de différenciation myéloïde-88</term>
<term>Lymphocytes</term>
<term>Lésion pulmonaire</term>
<term>Poumon</term>
<term>Protéines associées aux microtubules</term>
<term>Récepteur de type Toll-4</term>
<term>Sérine-thréonine kinases TOR</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term>
<term>Lung Injury</term>
<term>Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="induit chimiquement" xml:lang="fr"><term>Lésion pulmonaire</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
<term>Lung Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Thiénamycine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Thienamycins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Particulate Matter</term>
</keywords>
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<term>Bronchoalveolar Lavage</term>
<term>Drug Repositioning</term>
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<term>Mice</term>
<term>Mice, Inbred BALB C</term>
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<term>Lavage bronchoalvéolaire</term>
<term>Mâle</term>
<term>Repositionnement des médicaments</term>
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<front><div type="abstract" xml:lang="en">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 (PM<sub>2.5</sub>
) 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 PM<sub>2.5</sub>
. 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 PM<sub>2.5</sub>
-treated mice. BIPM effectively reduced the pathological lung injury, lung wet/dry weight ratio, and hyperpermeability caused by PM<sub>2.5</sub>
. Enhanced myeloperoxidase (MPO) activity by PM<sub>2.5</sub>
 in the pulmonary tissue was inhibited by BIPM. Moreover, increased levels of inflammatory cytokines and total protein by PM<sub>2.5</sub>
 in the BALF were also decreased by BIPM treatment. In addition, BIPM markedly suppressed PM<sub>2.5</sub>
-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 PM<sub>2.5</sub>
 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 PM<sub>2.5</sub>
-induced pulmonary injury.</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>11</Month>
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<Abstract><AbstractText>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 (PM<sub>2.5</sub>
) 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 PM<sub>2.5</sub>
. 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 PM<sub>2.5</sub>
-treated mice. BIPM effectively reduced the pathological lung injury, lung wet/dry weight ratio, and hyperpermeability caused by PM<sub>2.5</sub>
. Enhanced myeloperoxidase (MPO) activity by PM<sub>2.5</sub>
 in the pulmonary tissue was inhibited by BIPM. Moreover, increased levels of inflammatory cytokines and total protein by PM<sub>2.5</sub>
 in the BALF were also decreased by BIPM treatment. In addition, BIPM markedly suppressed PM<sub>2.5</sub>
-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 PM<sub>2.5</sub>
 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 PM<sub>2.5</sub>
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Biapenem as a Novel Insight into Drug Repositioning against Particulate Matter-Induced Lung Injury.

Biapenem as a Novel Insight into Drug Repositioning against Particulate Matter-Induced Lung Injury.

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