ChloroquineV1, PubMed, Checkpoint, bibRecord, 000174

Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.

Identifieur interne : 000174 ( PubMed/Checkpoint ); précédent : 000173; suivant : 000175

Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.

Auteurs : Li Liu [République populaire de Chine] ; Jun Ren [République populaire de Chine] ; Zhiyao He [République populaire de Chine] ; Ke Men [République populaire de Chine] ; Ye Mao [République populaire de Chine] ; Tinghong Ye [République populaire de Chine] ; Hua Chen [République populaire de Chine] ; Ling Li [République populaire de Chine] ; Bocheng Xu [République populaire de Chine] ; Yuquan Wei [République populaire de Chine] ; Xiawei Wei [République populaire de Chine]

Source :

Scientific reports [ 2045-2322 ] ; 2017.

RBID : pubmed:28878315

Descripteurs français

KwdFr :
- Animaux, Apoptose (), Bléomycine (effets indésirables), Cholestérol (), Cytokines (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Femelle, Fibroblastes (métabolisme), Fibrose pulmonaire (anatomopathologie), Fibrose pulmonaire (traitement médicamenteux), Fibrose pulmonaire (étiologie), Hydroxychloroquine (), Hydroxychloroquine (administration et posologie), Immunohistochimie, Liposomes (), Marqueurs biologiques, Modèles animaux de maladie humaine, Nanoparticules (), Phosphorylation, Rats, Spectroscopie par résonance magnétique, Structure moléculaire, Système de signalisation des MAP kinases (), Systèmes de délivrance de médicaments, Transduction du signal, Vecteurs de médicaments ().
MESH :
- administration et posologie : Hydroxychloroquine.
- anatomopathologie : Fibrose pulmonaire.
- effets indésirables : Bléomycine.
- métabolisme : Cytokines, Facteur de transcription NF-kappa B, Fibroblastes.
- traitement médicamenteux : Fibrose pulmonaire.
- étiologie : Fibrose pulmonaire.
- Animaux, Apoptose, Cholestérol, Femelle, Hydroxychloroquine, Immunohistochimie, Liposomes, Marqueurs biologiques, Modèles animaux de maladie humaine, Nanoparticules, Phosphorylation, Rats, Spectroscopie par résonance magnétique, Structure moléculaire, Système de signalisation des MAP kinases, Systèmes de délivrance de médicaments, Transduction du signal, Vecteurs de médicaments.

English descriptors

KwdEn :
- Animals, Apoptosis (drug effects), Biomarkers, Bleomycin (adverse effects), Cholesterol (chemistry), Cytokines (metabolism), Disease Models, Animal, Drug Carriers (chemistry), Drug Delivery Systems, Female, Fibroblasts (metabolism), Hydroxychloroquine (administration & dosage), Hydroxychloroquine (chemistry), Immunohistochemistry, Liposomes (chemistry), MAP Kinase Signaling System (drug effects), Magnetic Resonance Spectroscopy, Molecular Structure, NF-kappa B (metabolism), Nanoparticles (chemistry), Phosphorylation, Pulmonary Fibrosis (drug therapy), Pulmonary Fibrosis (etiology), Pulmonary Fibrosis (pathology), Rats, Signal Transduction.
MESH :
- chemical , administration & dosage : Hydroxychloroquine.
- chemical , adverse effects : Bleomycin.
- chemical , chemistry : Cholesterol, Drug Carriers, Hydroxychloroquine, Liposomes.
- chemical , metabolism : Cytokines, NF-kappa B.
- chemical : Biomarkers.
- chemistry : Nanoparticles.
- drug effects : Apoptosis, MAP Kinase Signaling System.
- drug therapy : Pulmonary Fibrosis.
- etiology : Pulmonary Fibrosis.
- metabolism : Fibroblasts.
- pathology : Pulmonary Fibrosis.
- Animals, Disease Models, Animal, Drug Delivery Systems, Female, Immunohistochemistry, Magnetic Resonance Spectroscopy, Molecular Structure, Phosphorylation, Rats, Signal Transduction.

Abstract

An increasing number of reports have suggested the use of hydroxychloroquine (HCQ) as an adjunct anti-cancer treatment to enhance the chemotherapeutic response, as well as for the treatment of several fibrotic skin diseases and cystic fibrosis. In this study, we synthesized a cholesterol-modified HCQ (Chol-HCQ) and hypothesized that a systemic delivery system with Chol-HCQ nanocarriers could be effective for the treatment of bleomycin-induced pulmonary fibrosis. Chol-HCQ significantly inhibits the proliferation of rat lung fibroblasts, regulates inflammation and ameliorates bleomycin-induced pulmonary fibrosis in rats. It regulates the expression of pro-inflammatory cytokines, such as TNF-α; reduces the infiltration of inflammatory neutrophils; and inhibits the phosphorylation of NF-κB. Chol-HCQ also reduces the expression of connective tissue growth factor (CTGF) and phosphorylation of extracellular regulated protein kinase (p-ERK) in rats with bleomycin-induced pulmonary fibrosis. Chol-HCQ nanocarriers reduce early pulmonary inflammation and inhibit the CTGF/ERK signalling pathway in bleomycin-induced pulmonary fibrosis. These results demonstrate that Chol-HCQ liposomes suppress pulmonary inflammation and reduce pulmonary fibrosis induced by bleomycin. The systemic administration safety of Chol-HCQ liposomes was confirmed after intravenous administration for 28 days in rats. The present study provides evidence that Chol-HCQ liposomes may be a potential therapeutic agent for inflammation associated with pulmonary fibrosis.

DOI: 10.1038/s41598-017-11450-3
PubMed: 28878315

Affiliations:

République populaire de Chine

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Apoptosis (drug effects)</term>
<term>Biomarkers</term>
<term>Bleomycin (adverse effects)</term>
<term>Cholesterol (chemistry)</term>
<term>Cytokines (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Drug Carriers (chemistry)</term>
<term>Drug Delivery Systems</term>
<term>Female</term>
<term>Fibroblasts (metabolism)</term>
<term>Hydroxychloroquine (administration & dosage)</term>
<term>Hydroxychloroquine (chemistry)</term>
<term>Immunohistochemistry</term>
<term>Liposomes (chemistry)</term>
<term>MAP Kinase Signaling System (drug effects)</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Molecular Structure</term>
<term>NF-kappa B (metabolism)</term>
<term>Nanoparticles (chemistry)</term>
<term>Phosphorylation</term>
<term>Pulmonary Fibrosis (drug therapy)</term>
<term>Pulmonary Fibrosis (etiology)</term>
<term>Pulmonary Fibrosis (pathology)</term>
<term>Rats</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose ()</term>
<term>Bléomycine (effets indésirables)</term>
<term>Cholestérol ()</term>
<term>Cytokines (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Femelle</term>
<term>Fibroblastes (métabolisme)</term>
<term>Fibrose pulmonaire (anatomopathologie)</term>
<term>Fibrose pulmonaire (traitement médicamenteux)</term>
<term>Fibrose pulmonaire (étiologie)</term>
<term>Hydroxychloroquine ()</term>
<term>Hydroxychloroquine (administration et posologie)</term>
<term>Immunohistochimie</term>
<term>Liposomes ()</term>
<term>Marqueurs biologiques</term>
<term>Modèles animaux de maladie humaine</term>
<term>Nanoparticules ()</term>
<term>Phosphorylation</term>
<term>Rats</term>
<term>Spectroscopie par résonance magnétique</term>
<term>Structure moléculaire</term>
<term>Système de signalisation des MAP kinases ()</term>
<term>Systèmes de délivrance de médicaments</term>
<term>Transduction du signal</term>
<term>Vecteurs de médicaments ()</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Hydroxychloroquine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Bleomycin</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Cholesterol</term>
<term>Drug Carriers</term>
<term>Hydroxychloroquine</term>
<term>Liposomes</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
<term>NF-kappa B</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biomarkers</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Hydroxychloroquine</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Fibrose pulmonaire</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Nanoparticles</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>MAP Kinase Signaling System</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Pulmonary Fibrosis</term>
</keywords>
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<term>Facteur de transcription NF-kappa B</term>
<term>Fibroblastes</term>
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<term>Disease Models, Animal</term>
<term>Drug Delivery Systems</term>
<term>Female</term>
<term>Immunohistochemistry</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Molecular Structure</term>
<term>Phosphorylation</term>
<term>Rats</term>
<term>Signal Transduction</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cholestérol</term>
<term>Femelle</term>
<term>Hydroxychloroquine</term>
<term>Immunohistochimie</term>
<term>Liposomes</term>
<term>Marqueurs biologiques</term>
<term>Modèles animaux de maladie humaine</term>
<term>Nanoparticules</term>
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<term>Rats</term>
<term>Spectroscopie par résonance magnétique</term>
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<term>Système de signalisation des MAP kinases</term>
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<front><div type="abstract" xml:lang="en">An increasing number of reports have suggested the use of hydroxychloroquine (HCQ) as an adjunct anti-cancer treatment to enhance the chemotherapeutic response, as well as for the treatment of several fibrotic skin diseases and cystic fibrosis. In this study, we synthesized a cholesterol-modified HCQ (Chol-HCQ) and hypothesized that a systemic delivery system with Chol-HCQ nanocarriers could be effective for the treatment of bleomycin-induced pulmonary fibrosis. Chol-HCQ significantly inhibits the proliferation of rat lung fibroblasts, regulates inflammation and ameliorates bleomycin-induced pulmonary fibrosis in rats. It regulates the expression of pro-inflammatory cytokines, such as TNF-α; reduces the infiltration of inflammatory neutrophils; and inhibits the phosphorylation of NF-κB. Chol-HCQ also reduces the expression of connective tissue growth factor (CTGF) and phosphorylation of extracellular regulated protein kinase (p-ERK) in rats with bleomycin-induced pulmonary fibrosis. Chol-HCQ nanocarriers reduce early pulmonary inflammation and inhibit the CTGF/ERK signalling pathway in bleomycin-induced pulmonary fibrosis. These results demonstrate that Chol-HCQ liposomes suppress pulmonary inflammation and reduce pulmonary fibrosis induced by bleomycin. The systemic administration safety of Chol-HCQ liposomes was confirmed after intravenous administration for 28 days in rats. The present study provides evidence that Chol-HCQ liposomes may be a potential therapeutic agent for inflammation associated with pulmonary fibrosis.</div>
</front>
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<DateCompleted><Year>2019</Year>
<Month>05</Month>
<Day>13</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>05</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>1</Issue>
<PubDate><Year>2017</Year>
<Month>09</Month>
<Day>06</Day>
</PubDate>
</JournalIssue>
<Title>Scientific reports</Title>
<ISOAbbreviation>Sci Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.</ArticleTitle>
<Pagination><MedlinePgn>10737</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-017-11450-3</ELocationID>
<Abstract><AbstractText>An increasing number of reports have suggested the use of hydroxychloroquine (HCQ) as an adjunct anti-cancer treatment to enhance the chemotherapeutic response, as well as for the treatment of several fibrotic skin diseases and cystic fibrosis. In this study, we synthesized a cholesterol-modified HCQ (Chol-HCQ) and hypothesized that a systemic delivery system with Chol-HCQ nanocarriers could be effective for the treatment of bleomycin-induced pulmonary fibrosis. Chol-HCQ significantly inhibits the proliferation of rat lung fibroblasts, regulates inflammation and ameliorates bleomycin-induced pulmonary fibrosis in rats. It regulates the expression of pro-inflammatory cytokines, such as TNF-α; reduces the infiltration of inflammatory neutrophils; and inhibits the phosphorylation of NF-κB. Chol-HCQ also reduces the expression of connective tissue growth factor (CTGF) and phosphorylation of extracellular regulated protein kinase (p-ERK) in rats with bleomycin-induced pulmonary fibrosis. Chol-HCQ nanocarriers reduce early pulmonary inflammation and inhibit the CTGF/ERK signalling pathway in bleomycin-induced pulmonary fibrosis. These results demonstrate that Chol-HCQ liposomes suppress pulmonary inflammation and reduce pulmonary fibrosis induced by bleomycin. The systemic administration safety of Chol-HCQ liposomes was confirmed after intravenous administration for 28 days in rats. The present study provides evidence that Chol-HCQ liposomes may be a potential therapeutic agent for inflammation associated with pulmonary fibrosis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Li</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ren</LastName>
<ForeName>Jun</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>He</LastName>
<ForeName>Zhiyao</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Men</LastName>
<ForeName>Ke</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mao</LastName>
<ForeName>Ye</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Ye</LastName>
<ForeName>Tinghong</ForeName>
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<Identifier Source="ORCID">0000-0002-3296-6753</Identifier>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Hua</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Ling</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Bocheng</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wei</LastName>
<ForeName>Yuquan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China. yqwei@scu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wei</LastName>
<ForeName>Xiawei</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy/Collaborative Innovation Centre, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, Sichuan, 610041, China. xiaweiwei@scu.edu.cn.</Affiliation>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>09</Month>
<Day>06</Day>
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<CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Am J Respir Crit Care Med. 2019 Jun 15;199(12):1561-1563</RefSource>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
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<MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName>
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<name sortKey="Wei, Xiawei" sort="Wei, Xiawei" uniqKey="Wei X" first="Xiawei" last="Wei">Xiawei Wei</name>
<name sortKey="Wei, Yuquan" sort="Wei, Yuquan" uniqKey="Wei Y" first="Yuquan" last="Wei">Yuquan Wei</name>
<name sortKey="Xu, Bocheng" sort="Xu, Bocheng" uniqKey="Xu B" first="Bocheng" last="Xu">Bocheng Xu</name>
<name sortKey="Ye, Tinghong" sort="Ye, Tinghong" uniqKey="Ye T" first="Tinghong" last="Ye">Tinghong Ye</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Checkpoint

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000174 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 000174 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    PubMed
   |étape=   Checkpoint
   |type=    RBID
   |clé=     pubmed:28878315
   |texte=   Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i   -Sk "pubmed:28878315" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a ChloroquineV1

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021

	Serveur d'exploration Chloroquine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration Chloroquine

Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.

Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.

Source :

Descripteurs français

English descriptors

Abstract

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

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki