ChloroquineV1, PubMed, Checkpoint, bibRecord, 000067

Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.

Identifieur interne : 000067 ( PubMed/Checkpoint ); précédent : 000066; suivant : 000068

Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.

Auteurs : Hongying Zhao [République populaire de Chine] ; Hongguang Chen [République populaire de Chine] ; Meng Xiaoyin [République populaire de Chine] ; Guotao Yang [République populaire de Chine] ; Ying Hu [République populaire de Chine] ; Keliang Xie [République populaire de Chine] ; Yonghao Yu [République populaire de Chine]

Source :

Inflammation [ 1573-2576 ] ; 2019.

RBID : pubmed:30645707

Descripteurs français

KwdFr :
- Animaux, Autophagie (physiologie), Bécline-1 (métabolisme), Cytokines (métabolisme), Inflammation (), Lésion pulmonaire aigüe (), Modèles animaux de maladie humaine, Protéine de membrane-2 associée au lysosome (métabolisme), Protéines G rab (métabolisme), Protéines associées aux microtubules, Sepsie (), Sepsie (anatomopathologie), Souris, Taux de survie.
MESH :
- anatomopathologie : Sepsie.
- métabolisme : Bécline-1, Cytokines, Protéine de membrane-2 associée au lysosome, Protéines G rab.
- physiologie : Autophagie.
- Animaux, Inflammation, Lésion pulmonaire aigüe, Modèles animaux de maladie humaine, Protéines associées aux microtubules, Sepsie, Souris, Taux de survie.

English descriptors

KwdEn :
- Acute Lung Injury (prevention & control), Animals, Autophagy (physiology), Beclin-1 (metabolism), Cytokines (metabolism), Disease Models, Animal, Inflammation (prevention & control), Lysosomal-Associated Membrane Protein 2 (metabolism), Mice, Microtubule-Associated Proteins, Sepsis (complications), Sepsis (pathology), Survival Rate, rab GTP-Binding Proteins (metabolism).
MESH :
- chemical , metabolism : Beclin-1, Cytokines, Lysosomal-Associated Membrane Protein 2, rab GTP-Binding Proteins.
- complications : Sepsis.
- pathology : Sepsis.
- physiology : Autophagy.
- prevention & control : Acute Lung Injury, Inflammation.
- Animals, Disease Models, Animal, Mice, Microtubule-Associated Proteins, Survival Rate.

Abstract

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) undergoes the process of pathological event including lung tissue dysfunction, pulmonary edema, and inflammation in sepsis. Autophagy is a cytoprotective process recognized as one of the major pathways for degradation and recycling of cellular constituents. Autophagy as a protective or maladaptive response was still confused in ALI during sepsis. Acute lung injury was performed by cecal ligation and puncture (CLP). Autophagic inducer rapacymin and inhibitor 3-MA and autophagosomal-lysosome fusion inhibitor bafilomucin (Baf) A1 and chloroquine (CQ) were administrated by intraperitoneal injection at 1 h after CLP operation. Microtubule-associated protein light chain 3 II (LC3II), Beclin 1, Rab7, and lysosome-associated membrane protein type 2 (LAMP2) were detected by western blotting. Seven-day survival rate of septic mice was observed. Histologic scores, lung wet-to-dry (W/D) weight ratio, oxygenation index (PaO₂/FiO₂), total cells and polymorphonuclear neutrophils (PMN) in bronchial alveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity and cytokine tumor necrosis factor (TNF)-α, high-mobility group box (HMGB)1, interleukin (IL)-6, IL-10, and monocyte chemotactic protein (MCP)1 were measured after sham or ALI operation. ALI induced the increasing expression of autophagy-related protein LC3II, Beclin 1, Rab7, and LAMP2 in CLP operation. Autophagic inducer rapacymin significantly induced the expression of LC3II, Beclin 1, LAMP2, and Rab7 in mice model of CLP, and inhibitor 3-MA reduced expression of LC3II, Beclin 1, LAMP2, and Rab7 expressions in CLP + RAP mice compared to CLP group. Compared with ALI group, Baf and CQ obviously elevated the level of LC3II and Beclin 1, and reduced the LAMP2 and Rab7 expressions in CLP + Baf group and ALI + CQ group. Compared with CLP group, autophagic inducer rapacymin improved the survival rate, histologic scores, lung wet/dry weight ratio, PaO₂/FiO₂, total cells, and PMNS in BALF and MPO activity and cytokines TNF-α, HMGB1, IL-6, IL-10, and MCP1 in CLP + RAP group, but there were exacerbated above indicators in CLP + 3-MA group, CLP + Baf group, and CLP + CQ group. Autophagy activation participated in the pathophysiologic process of sepsis, and alleviated the cytokine excessive release and lung injury in sepsis.

DOI: 10.1007/s10753-018-00952-5
PubMed: 30645707

Affiliations:

République populaire de Chine

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<term>Cytokines (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Inflammation (prevention & control)</term>
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<term>Protéines G rab</term>
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<front><div type="abstract" xml:lang="en">Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) undergoes the process of pathological event including lung tissue dysfunction, pulmonary edema, and inflammation in sepsis. Autophagy is a cytoprotective process recognized as one of the major pathways for degradation and recycling of cellular constituents. Autophagy as a protective or maladaptive response was still confused in ALI during sepsis. Acute lung injury was performed by cecal ligation and puncture (CLP). Autophagic inducer rapacymin and inhibitor 3-MA and autophagosomal-lysosome fusion inhibitor bafilomucin (Baf) A1 and chloroquine (CQ) were administrated by intraperitoneal injection at 1 h after CLP operation. Microtubule-associated protein light chain 3 II (LC3II), Beclin 1, Rab7, and lysosome-associated membrane protein type 2 (LAMP2) were detected by western blotting. Seven-day survival rate of septic mice was observed. Histologic scores, lung wet-to-dry (W/D) weight ratio, oxygenation index (PaO<sub>2</sub>
/FiO<sub>2</sub>
), total cells and polymorphonuclear neutrophils (PMN) in bronchial alveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity and cytokine tumor necrosis factor (TNF)-α, high-mobility group box (HMGB)1, interleukin (IL)-6, IL-10, and monocyte chemotactic protein (MCP)1 were measured after sham or ALI operation. ALI induced the increasing expression of autophagy-related protein LC3II, Beclin 1, Rab7, and LAMP2 in CLP operation. Autophagic inducer rapacymin significantly induced the expression of LC3II, Beclin 1, LAMP2, and Rab7 in mice model of CLP, and inhibitor 3-MA reduced expression of LC3II, Beclin 1, LAMP2, and Rab7 expressions in CLP + RAP mice compared to CLP group. Compared with ALI group, Baf and CQ obviously elevated the level of LC3II and Beclin 1, and reduced the LAMP2 and Rab7 expressions in CLP + Baf group and ALI + CQ group. Compared with CLP group, autophagic inducer rapacymin improved the survival rate, histologic scores, lung wet/dry weight ratio, PaO<sub>2</sub>
/FiO<sub>2</sub>
, total cells, and PMNS in BALF and MPO activity and cytokines TNF-α, HMGB1, IL-6, IL-10, and MCP1 in CLP + RAP group, but there were exacerbated above indicators in CLP + 3-MA group, CLP + Baf group, and CLP + CQ group. Autophagy activation participated in the pathophysiologic process of sepsis, and alleviated the cytokine excessive release and lung injury in sepsis.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30645707</PMID>
<DateCompleted><Year>2019</Year>
<Month>08</Month>
<Day>02</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-2576</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>42</Volume>
<Issue>2</Issue>
<PubDate><Year>2019</Year>
<Month>Apr</Month>
</PubDate>
</JournalIssue>
<Title>Inflammation</Title>
<ISOAbbreviation>Inflammation</ISOAbbreviation>
</Journal>
<ArticleTitle>Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.</ArticleTitle>
<Pagination><MedlinePgn>426-439</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s10753-018-00952-5</ELocationID>
<Abstract><AbstractText>Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) undergoes the process of pathological event including lung tissue dysfunction, pulmonary edema, and inflammation in sepsis. Autophagy is a cytoprotective process recognized as one of the major pathways for degradation and recycling of cellular constituents. Autophagy as a protective or maladaptive response was still confused in ALI during sepsis. Acute lung injury was performed by cecal ligation and puncture (CLP). Autophagic inducer rapacymin and inhibitor 3-MA and autophagosomal-lysosome fusion inhibitor bafilomucin (Baf) A1 and chloroquine (CQ) were administrated by intraperitoneal injection at 1 h after CLP operation. Microtubule-associated protein light chain 3 II (LC3II), Beclin 1, Rab7, and lysosome-associated membrane protein type 2 (LAMP2) were detected by western blotting. Seven-day survival rate of septic mice was observed. Histologic scores, lung wet-to-dry (W/D) weight ratio, oxygenation index (PaO<sub>2</sub>
/FiO<sub>2</sub>
), total cells and polymorphonuclear neutrophils (PMN) in bronchial alveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity and cytokine tumor necrosis factor (TNF)-α, high-mobility group box (HMGB)1, interleukin (IL)-6, IL-10, and monocyte chemotactic protein (MCP)1 were measured after sham or ALI operation. ALI induced the increasing expression of autophagy-related protein LC3II, Beclin 1, Rab7, and LAMP2 in CLP operation. Autophagic inducer rapacymin significantly induced the expression of LC3II, Beclin 1, LAMP2, and Rab7 in mice model of CLP, and inhibitor 3-MA reduced expression of LC3II, Beclin 1, LAMP2, and Rab7 expressions in CLP + RAP mice compared to CLP group. Compared with ALI group, Baf and CQ obviously elevated the level of LC3II and Beclin 1, and reduced the LAMP2 and Rab7 expressions in CLP + Baf group and ALI + CQ group. Compared with CLP group, autophagic inducer rapacymin improved the survival rate, histologic scores, lung wet/dry weight ratio, PaO<sub>2</sub>
/FiO<sub>2</sub>
, total cells, and PMNS in BALF and MPO activity and cytokines TNF-α, HMGB1, IL-6, IL-10, and MCP1 in CLP + RAP group, but there were exacerbated above indicators in CLP + 3-MA group, CLP + Baf group, and CLP + CQ group. Autophagy activation participated in the pathophysiologic process of sepsis, and alleviated the cytokine excessive release and lung injury in sepsis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Hongying</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Geriatric, Cangzhou Central Hospital, Cangzhou City, Hebei Province, 061001, People's Republic of China. 147954295@qq.com.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Hongguang</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, Tianjin, 300052, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xiaoyin</LastName>
<ForeName>Meng</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Gynecology and Obstetrics, Tianjin Hospital, Tianjin, 300211, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Guotao</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, Cangzhou Central Hospital, Cangzhou City, Hebei Province, 061001, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Ying</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Anesthesiology, Children's Hospital of Zhengzhou, Zhengzhou, Henan, 50053, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xie</LastName>
<ForeName>Keliang</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, Tianjin, 300052, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yu</LastName>
<ForeName>Yonghao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, Tianjin, 300052, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>81471842,81772043</GrantID>
<Agency>the National Natural Science Foundation of China</Agency>
<Country></Country>
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Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.

Autophagy Activation Improves Lung Injury and Inflammation in Sepsis.

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