Serveur d'exploration Chloroquine

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

Identifieur interne : 000D23 ( Main/Exploration ); précédent : 000D22; suivant : 000D24

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 :

RBID : pubmed:28878315

Descripteurs français

English descriptors

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


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<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>
<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>
</textClass>
</profileDesc>
</teiHeader>
<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>
</TEI>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Liu, Li" sort="Liu, Li" uniqKey="Liu L" first="Li" last="Liu">Li Liu</name>
</noRegion>
<name sortKey="Chen, Hua" sort="Chen, Hua" uniqKey="Chen H" first="Hua" last="Chen">Hua Chen</name>
<name sortKey="He, Zhiyao" sort="He, Zhiyao" uniqKey="He Z" first="Zhiyao" last="He">Zhiyao He</name>
<name sortKey="Li, Ling" sort="Li, Ling" uniqKey="Li L" first="Ling" last="Li">Ling Li</name>
<name sortKey="Mao, Ye" sort="Mao, Ye" uniqKey="Mao Y" first="Ye" last="Mao">Ye Mao</name>
<name sortKey="Men, Ke" sort="Men, Ke" uniqKey="Men K" first="Ke" last="Men">Ke Men</name>
<name sortKey="Ren, Jun" sort="Ren, Jun" uniqKey="Ren J" first="Jun" last="Ren">Jun Ren</name>
<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>

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