Chloroquine attenuates paraquat-induced lung injury in mice by altering inflammation, oxidative stress and fibrosis.
Identifieur interne : 000D24 ( Main/Exploration ); précédent : 000D23; suivant : 000D25Chloroquine attenuates paraquat-induced lung injury in mice by altering inflammation, oxidative stress and fibrosis.
Auteurs : Haitao Shen [République populaire de Chine] ; Na Wu [République populaire de Chine] ; Yu Wang [République populaire de Chine] ; Hongyu Zhao [République populaire de Chine] ; Lichun Zhang [République populaire de Chine] ; Tiegang Li [République populaire de Chine] ; Min Zhao [République populaire de Chine]Source :
- International immunopharmacology [ 1878-1705 ] ; 2017.
Descripteurs français
- KwdFr :
- Actines (métabolisme), Animaux, Anti-inflammatoires (usage thérapeutique), Chloroquine (usage thérapeutique), Cytokines (métabolisme), Facteur-2 apparenté à NF-E2 (métabolisme), Fibrose pulmonaire (), Fibrose pulmonaire (traitement médicamenteux), Humains, Inflammation (), Inflammation (traitement médicamenteux), Lésion pulmonaire aigüe (), Lésion pulmonaire aigüe (traitement médicamenteux), Mâle, Médiateurs de l'inflammation (métabolisme), Paraquat, Poumon (), Poumon (immunologie), Souris, Souris de lignée C57BL, Stress oxydatif (), Superoxide dismutase-1 (métabolisme).
- MESH :
- immunologie : Poumon.
- métabolisme : Actines, Cytokines, Facteur-2 apparenté à NF-E2, Médiateurs de l'inflammation, Superoxide dismutase-1.
- traitement médicamenteux : Fibrose pulmonaire, Inflammation, Lésion pulmonaire aigüe.
- usage thérapeutique : Anti-inflammatoires, Chloroquine.
- Animaux, Fibrose pulmonaire, Humains, Inflammation, Lésion pulmonaire aigüe, Mâle, Paraquat, Poumon, Souris, Souris de lignée C57BL, Stress oxydatif.
English descriptors
- KwdEn :
- Actins (metabolism), Acute Lung Injury (chemically induced), Acute Lung Injury (drug therapy), Animals, Anti-Inflammatory Agents (therapeutic use), Chloroquine (therapeutic use), Cytokines (metabolism), Humans, Inflammation (chemically induced), Inflammation (drug therapy), Inflammation Mediators (metabolism), Lung (drug effects), Lung (immunology), Male, Mice, Mice, Inbred C57BL, NF-E2-Related Factor 2 (metabolism), Oxidative Stress (drug effects), Paraquat, Pulmonary Fibrosis (chemically induced), Pulmonary Fibrosis (drug therapy), Superoxide Dismutase-1 (metabolism).
- MESH :
- chemical , metabolism : Actins, Cytokines, Inflammation Mediators, NF-E2-Related Factor 2, Superoxide Dismutase-1.
- chemically induced : Acute Lung Injury, Inflammation, Pulmonary Fibrosis.
- drug effects : Lung, Oxidative Stress.
- drug therapy : Acute Lung Injury, Inflammation, Pulmonary Fibrosis.
- immunology : Lung.
- chemical , therapeutic use : Anti-Inflammatory Agents, Chloroquine.
- Animals, Humans, Male, Mice, Mice, Inbred C57BL, Paraquat.
Abstract
Paraquat is one of the most extensively used herbicides and has high toxicity for humans and animals. However, there is no effective treatment for paraquat poisoning. The aim of the present study was to evaluate the effects of chloroquine on paraquat-induced lung injury in mice. Mice received a single intraperitoneal injection of paraquat and a daily intraperitoneal injection of the indicated dosages of chloroquine or dexamethasone. The histological changes, inflammation and oxidative stress in the lungs were examined at day 3, and the degree of pulmonary fibrosis was examined at day 28. H&E staining showed that chloroquine markedly attenuated lung injury induced by paraquat. In addition, the inflammatory responses induced by paraquat were inhibited after treatment with chloroquine, as indicated by the decreased number of leukocytes, the reduced levels of TNF-α, IL-1β and IL-6 in the bronchoalveolar lavage fluid, the reduced NO content, and downregulation of iNOS expression in lung tissues. No different effect was found between high-dose chloroquine and dexamethasone. Additionally, the treatment with chloroquine increased the activity of SOD and decreased the level of MDA in the lung tissues. The expressions of the anti-oxidative proteins, Nrf2, HO-1 and NQO1, were also upregulated by chloroquine treatment. The high-dose chloroquine was more effective than dexamethasone in its anti-oxidation ability. Finally, the results of Masson's staining illustrated that chloroquine markedly attenuated fibrosis in the paraquat-exposed lungs. Immunohistochemistry staining showed that the expressions of the pro-fibrotic proteins TGF-β and α-SMA were downregulated after treatment with chloroquine. In conclusion, chloroquine effectively attenuated paraquat-induced lung injury in mice.
DOI: 10.1016/j.intimp.2017.02.020
PubMed: 28249220
Affiliations:
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110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Na" sort="Wu, Na" uniqKey="Wu N" first="Na" last="Wu">Na Wu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang 110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Yu" sort="Wang, Yu" uniqKey="Wang Y" first="Yu" last="Wang">Yu Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Hongyu" sort="Zhao, Hongyu" uniqKey="Zhao H" first="Hongyu" last="Zhao">Hongyu Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Lichun" sort="Zhang, Lichun" uniqKey="Zhang L" first="Lichun" last="Zhang">Lichun Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author><author><name sortKey="Li, Tiegang" sort="Li, Tiegang" uniqKey="Li T" first="Tiegang" last="Li">Tiegang Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Min" sort="Zhao, Min" uniqKey="Zhao M" first="Min" last="Zhao">Min Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China. Electronic address: zhaom@sj-hospital.org.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004</wicri:regionArea><wicri:noRegion>Shenyang 110004</wicri:noRegion></affiliation></author></analytic><series><title level="j">International immunopharmacology</title><idno type="eISSN">1878-1705</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Actins (metabolism)</term><term>Acute Lung Injury (chemically induced)</term><term>Acute Lung Injury (drug therapy)</term><term>Animals</term><term>Anti-Inflammatory Agents (therapeutic use)</term><term>Chloroquine (therapeutic use)</term><term>Cytokines (metabolism)</term><term>Humans</term><term>Inflammation (chemically induced)</term><term>Inflammation (drug therapy)</term><term>Inflammation Mediators (metabolism)</term><term>Lung (drug effects)</term><term>Lung (immunology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>NF-E2-Related Factor 2 (metabolism)</term><term>Oxidative Stress (drug effects)</term><term>Paraquat</term><term>Pulmonary Fibrosis (chemically induced)</term><term>Pulmonary Fibrosis (drug therapy)</term><term>Superoxide Dismutase-1 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Actines (métabolisme)</term><term>Animaux</term><term>Anti-inflammatoires (usage thérapeutique)</term><term>Chloroquine (usage thérapeutique)</term><term>Cytokines (métabolisme)</term><term>Facteur-2 apparenté à NF-E2 (métabolisme)</term><term>Fibrose pulmonaire ()</term><term>Fibrose pulmonaire (traitement médicamenteux)</term><term>Humains</term><term>Inflammation ()</term><term>Inflammation (traitement médicamenteux)</term><term>Lésion pulmonaire aigüe ()</term><term>Lésion pulmonaire aigüe (traitement médicamenteux)</term><term>Mâle</term><term>Médiateurs de l'inflammation (métabolisme)</term><term>Paraquat</term><term>Poumon ()</term><term>Poumon (immunologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stress oxydatif ()</term><term>Superoxide dismutase-1 (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Actins</term><term>Cytokines</term><term>Inflammation Mediators</term><term>NF-E2-Related Factor 2</term><term>Superoxide Dismutase-1</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Acute Lung Injury</term><term>Inflammation</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lung</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Acute Lung Injury</term><term>Inflammation</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Actines</term><term>Cytokines</term><term>Facteur-2 apparenté à NF-E2</term><term>Médiateurs de l'inflammation</term><term>Superoxide dismutase-1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Fibrose pulmonaire</term><term>Inflammation</term><term>Lésion pulmonaire aigüe</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Anti-inflammatoires</term><term>Chloroquine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Paraquat</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Fibrose pulmonaire</term><term>Humains</term><term>Inflammation</term><term>Lésion pulmonaire aigüe</term><term>Mâle</term><term>Paraquat</term><term>Poumon</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stress oxydatif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Paraquat is one of the most extensively used herbicides and has high toxicity for humans and animals. However, there is no effective treatment for paraquat poisoning. The aim of the present study was to evaluate the effects of chloroquine on paraquat-induced lung injury in mice. Mice received a single intraperitoneal injection of paraquat and a daily intraperitoneal injection of the indicated dosages of chloroquine or dexamethasone. The histological changes, inflammation and oxidative stress in the lungs were examined at day 3, and the degree of pulmonary fibrosis was examined at day 28. H&E staining showed that chloroquine markedly attenuated lung injury induced by paraquat. In addition, the inflammatory responses induced by paraquat were inhibited after treatment with chloroquine, as indicated by the decreased number of leukocytes, the reduced levels of TNF-α, IL-1β and IL-6 in the bronchoalveolar lavage fluid, the reduced NO content, and downregulation of iNOS expression in lung tissues. No different effect was found between high-dose chloroquine and dexamethasone. Additionally, the treatment with chloroquine increased the activity of SOD and decreased the level of MDA in the lung tissues. The expressions of the anti-oxidative proteins, Nrf2, HO-1 and NQO1, were also upregulated by chloroquine treatment. The high-dose chloroquine was more effective than dexamethasone in its anti-oxidation ability. Finally, the results of Masson's staining illustrated that chloroquine markedly attenuated fibrosis in the paraquat-exposed lungs. Immunohistochemistry staining showed that the expressions of the pro-fibrotic proteins TGF-β and α-SMA were downregulated after treatment with chloroquine. In conclusion, chloroquine effectively attenuated paraquat-induced lung injury in mice.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Shen, Haitao" sort="Shen, Haitao" uniqKey="Shen H" first="Haitao" last="Shen">Haitao Shen</name></noRegion><name sortKey="Li, Tiegang" sort="Li, Tiegang" uniqKey="Li T" first="Tiegang" last="Li">Tiegang Li</name><name sortKey="Wang, Yu" sort="Wang, Yu" uniqKey="Wang Y" first="Yu" last="Wang">Yu Wang</name><name sortKey="Wu, Na" sort="Wu, Na" uniqKey="Wu N" first="Na" last="Wu">Na Wu</name><name sortKey="Zhang, Lichun" sort="Zhang, Lichun" uniqKey="Zhang L" first="Lichun" last="Zhang">Lichun Zhang</name><name sortKey="Zhao, Hongyu" sort="Zhao, Hongyu" uniqKey="Zhao H" first="Hongyu" last="Zhao">Hongyu Zhao</name><name sortKey="Zhao, Min" sort="Zhao, Min" uniqKey="Zhao M" first="Min" last="Zhao">Min Zhao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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