Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock
Identifieur interne : 002595 ( Main/Exploration ); précédent : 002594; suivant : 002596Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock
Auteurs : S. M Song [République populaire de Chine] ; S. M Lu [République populaire de Chine] ; Z. G Wang [République populaire de Chine] ; J. C Liu [République populaire de Chine] ; S. Q Guo [République populaire de Chine] ; Z. Li [République populaire de Chine]Source :
- Injury [ 0020-1383 ] ; 1999.
Descripteurs français
- KwdFr :
- Animaux, Antienzymes (usage thérapeutique), Chloroquine (usage thérapeutique), Chlorpromazine (usage thérapeutique), Choc septique (), Choc septique (anatomopathologie), Choc septique (enzymologie), Fluidité membranaire (), Fluidité membranaire (physiologie), Lapins, Membranes intracellulaires (), Membranes intracellulaires (physiologie), Mitochondries (), Mitochondries (physiologie), Phospholipases A (antagonistes et inhibiteurs), Phospholipases A (physiologie), Phospholipases A2.
- MESH :
- anatomopathologie : Choc septique.
- antagonistes et inhibiteurs : Phospholipases A.
- enzymologie : Choc septique.
- physiologie : Fluidité membranaire, Membranes intracellulaires, Mitochondries, Phospholipases A.
- usage thérapeutique : Antienzymes, Chloroquine, Chlorpromazine.
- Pascal (Inist)
- Animal, Animaux, Chloroquine, Chlorpromazine, Choc, Choc septique, Effet biologique, Endotoxémie, Fluidité, Fluidité membranaire, Fonction cellulaire, Inhibiteur enzyme, Lapin, Lapins, Membrane plasmique, Membranes intracellulaires, Mitochondrie, Mitochondries, Pathogénie, Phospholipases A2, Phénothiazine dérivé, Prétraitement, Survie, Trouble fonctionnel.
- Wicri :
- topic : Lapin.
English descriptors
- KwdEn :
- Animal, Animals, Biological effect, Cell function, Chloroquine, Chloroquine (therapeutic use), Chlorpromazine, Chlorpromazine (therapeutic use), Dysfunction, Endotoxemia, Enzyme Inhibitors (therapeutic use), Enzyme inhibitor, Fluidity, Intracellular Membranes (drug effects), Intracellular Membranes (physiology), Membrane Fluidity (drug effects), Membrane Fluidity (physiology), Mitochondria, Mitochondria (drug effects), Mitochondria (physiology), Pathogenesis, Phenothiazine derivatives, Phospholipases A (antagonists & inhibitors), Phospholipases A (physiology), Phospholipases A2, Plasma membrane, Pretreatment, Rabbit, Rabbits, Shock, Shock, Septic (enzymology), Shock, Septic (pathology), Shock, Septic (prevention & control), Survival.
- MESH :
- chemical , antagonists & inhibitors : Phospholipases A.
- chemical , physiology : Phospholipases A.
- chemical , therapeutic use : Chloroquine, Chlorpromazine, Enzyme Inhibitors.
- drug effects : Intracellular Membranes, Membrane Fluidity, Mitochondria.
- enzymology : Shock, Septic.
- pathology : Shock, Septic.
- physiology : Intracellular Membranes, Membrane Fluidity, Mitochondria.
- prevention & control : Shock, Septic.
- Animals, Phospholipases A2, Rabbits.
- Teeft :
- Acute lung injury, Arachidonic acid, Blood cells, Cellular damage, Cellular dysfunction, Chloroquine, Chlorpromazine, Distress syndrome, Elsevier science, Emission wave length, Endotoxin, Endotoxin administration, Endotoxin infusion, Endotoxin injection, Endotoxin shock, Fatty acids, Hitachi model, Inhibitor, Lipid, Lipid mediators, Lipid peroxidation, Lipid peroxides, Lipolytic enzyme, Liposome layer, Membrane, Membrane damage, Membrane microenvironment, Mitochondria membrane, Mitochondrion, Peroxidation, Phospholipase, Phospholipid, Pla2, Pla2 activity, Pla2 inhibitor, Pla2 inhibitors, Pla2 levels, Present study, Sepsis, Sepsis syndrome, Septic shock, Survival rate, Trauma surg, Uidity, Uorescence polarization.
Abstract
Abstract: The study aims at elucidating the mechanism involved in the cell dysfunction or impairment and the protective effects of phospholipase A2 (PLA2) inhibitors in endotoxin shock. Thirty-four rabbits were divided randomly into four groups: (1) normal control group (NC, n=6), receiving saline intravenously; (2) endotoxin shock group (ES, n=12), receiving 3mg/kg of E. coli endotoxin; (3) chloroquine pretreated group (CQ, n=8), receiving 3mg/kg of chloroquine 3min before endotoxin injection and (4) chlorpromazine pretreated group (CPZ, n=8), receiving 0.3mg/kg of chlorpromazine 30min before endotoxin injection. Hepatic mitochondria were extracted either 8h after commencement of the experiment or when the animals died for detecting PLA2 activity, membrane fluidity, membrane bound succinate dehydrogenate (SDH) and malondialdehyde (MDA). Mitochondria of the lung, heart and kidney were also used for detection of the membrane fluidity. It was revealed that the survival rate of 8h was 100% (NC), 58% (ES), 87.5% (CQ) and 75% (CPZ), respectively. Mean arterial pressure (MAP) dropped soon after endotoxin injection and descended continuously afterwards in the ES group (P<0.01). Fluorescence polarization, microviscosity and anisotrophy with a DPH probe were elevated above control levels (P<0.01). SDH was decreased obviously following endotoxin infusion (P<0.01). Chloroquine and chlorpromazine, serving as PLA2 inhibitors, could abate cellular dysfunction and increase survival rate. It is proposed that PLA2 plays a pivotal role in cellular injury in endotoxin shock. PLA2 inhibitor might serve as a useful adjunct in combating sepsis and shock.
Url:
DOI: 10.1016/S0020-1383(98)00178-8
Affiliations:
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Le document en format XML
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M" last="Song">S. M Song</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Surgery, 10 Changjiang Zhilu, Daping, Chongqing (400042)</wicri:regionArea><wicri:noRegion>Chongqing (400042)</wicri:noRegion></affiliation></author><author><name sortKey="Lu, S M" sort="Lu, S M" uniqKey="Lu S" first="S. M" last="Lu">S. M Lu</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Surgery, 10 Changjiang Zhilu, Daping, Chongqing (400042)</wicri:regionArea><wicri:noRegion>Chongqing (400042)</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Z G" sort="Wang, Z G" uniqKey="Wang Z" first="Z. G" last="Wang">Z. G Wang</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Surgery, 10 Changjiang Zhilu, Daping, Chongqing (400042)</wicri:regionArea><wicri:noRegion>Chongqing (400042)</wicri:noRegion></affiliation></author><author><name sortKey="Liu, J C" sort="Liu, J C" uniqKey="Liu J" first="J. C" last="Liu">J. C Liu</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Surgery, 10 Changjiang Zhilu, Daping, Chongqing (400042)</wicri:regionArea><wicri:noRegion>Chongqing (400042)</wicri:noRegion></affiliation></author><author><name sortKey="Guo, S Q" sort="Guo, S Q" uniqKey="Guo S" first="S. Q" last="Guo">S. Q Guo</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Surgery, 10 Changjiang Zhilu, Daping, Chongqing (400042)</wicri:regionArea><wicri:noRegion>Chongqing (400042)</wicri:noRegion></affiliation></author><author><name sortKey="Li, Z" sort="Li, Z" uniqKey="Li Z" first="Z" last="Li">Z. Li</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Surgery, 10 Changjiang Zhilu, Daping, Chongqing (400042)</wicri:regionArea><wicri:noRegion>Chongqing (400042)</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Injury</title><title level="j" type="abbrev">JINJ</title><idno type="ISSN">0020-1383</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999">1999</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="9">9</biblScope><biblScope unit="page" to="14">14</biblScope></imprint><idno type="ISSN">0020-1383</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0020-1383</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Animals</term><term>Biological effect</term><term>Cell function</term><term>Chloroquine</term><term>Chloroquine (therapeutic use)</term><term>Chlorpromazine</term><term>Chlorpromazine (therapeutic use)</term><term>Dysfunction</term><term>Endotoxemia</term><term>Enzyme Inhibitors (therapeutic use)</term><term>Enzyme inhibitor</term><term>Fluidity</term><term>Intracellular Membranes (drug effects)</term><term>Intracellular Membranes (physiology)</term><term>Membrane Fluidity (drug effects)</term><term>Membrane Fluidity (physiology)</term><term>Mitochondria</term><term>Mitochondria (drug effects)</term><term>Mitochondria (physiology)</term><term>Pathogenesis</term><term>Phenothiazine derivatives</term><term>Phospholipases A (antagonists & inhibitors)</term><term>Phospholipases A (physiology)</term><term>Phospholipases A2</term><term>Plasma membrane</term><term>Pretreatment</term><term>Rabbit</term><term>Rabbits</term><term>Shock</term><term>Shock, Septic (enzymology)</term><term>Shock, Septic (pathology)</term><term>Shock, Septic (prevention & control)</term><term>Survival</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antienzymes (usage thérapeutique)</term><term>Chloroquine (usage thérapeutique)</term><term>Chlorpromazine (usage thérapeutique)</term><term>Choc septique ()</term><term>Choc septique (anatomopathologie)</term><term>Choc septique (enzymologie)</term><term>Fluidité membranaire ()</term><term>Fluidité membranaire (physiologie)</term><term>Lapins</term><term>Membranes intracellulaires ()</term><term>Membranes intracellulaires (physiologie)</term><term>Mitochondries ()</term><term>Mitochondries (physiologie)</term><term>Phospholipases A (antagonistes et inhibiteurs)</term><term>Phospholipases A (physiologie)</term><term>Phospholipases A2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Phospholipases A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Phospholipases A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Chloroquine</term><term>Chlorpromazine</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Choc septique</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Phospholipases A</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Intracellular Membranes</term><term>Membrane Fluidity</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Choc septique</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Shock, Septic</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Shock, Septic</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Fluidité membranaire</term><term>Membranes intracellulaires</term><term>Mitochondries</term><term>Phospholipases A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Intracellular Membranes</term><term>Membrane Fluidity</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Shock, Septic</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antienzymes</term><term>Chloroquine</term><term>Chlorpromazine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Phospholipases A2</term><term>Rabbits</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Animal</term><term>Animaux</term><term>Chloroquine</term><term>Chlorpromazine</term><term>Choc</term><term>Choc septique</term><term>Effet biologique</term><term>Endotoxémie</term><term>Fluidité</term><term>Fluidité membranaire</term><term>Fonction cellulaire</term><term>Inhibiteur enzyme</term><term>Lapin</term><term>Lapins</term><term>Membrane plasmique</term><term>Membranes intracellulaires</term><term>Mitochondrie</term><term>Mitochondries</term><term>Pathogénie</term><term>Phospholipases A2</term><term>Phénothiazine dérivé</term><term>Prétraitement</term><term>Survie</term><term>Trouble fonctionnel</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Acute lung injury</term><term>Arachidonic acid</term><term>Blood cells</term><term>Cellular damage</term><term>Cellular dysfunction</term><term>Chloroquine</term><term>Chlorpromazine</term><term>Distress syndrome</term><term>Elsevier science</term><term>Emission wave length</term><term>Endotoxin</term><term>Endotoxin administration</term><term>Endotoxin infusion</term><term>Endotoxin injection</term><term>Endotoxin shock</term><term>Fatty acids</term><term>Hitachi model</term><term>Inhibitor</term><term>Lipid</term><term>Lipid mediators</term><term>Lipid peroxidation</term><term>Lipid peroxides</term><term>Lipolytic enzyme</term><term>Liposome layer</term><term>Membrane</term><term>Membrane damage</term><term>Membrane microenvironment</term><term>Mitochondria membrane</term><term>Mitochondrion</term><term>Peroxidation</term><term>Phospholipase</term><term>Phospholipid</term><term>Pla2</term><term>Pla2 activity</term><term>Pla2 inhibitor</term><term>Pla2 inhibitors</term><term>Pla2 levels</term><term>Present study</term><term>Sepsis</term><term>Sepsis syndrome</term><term>Septic shock</term><term>Survival rate</term><term>Trauma surg</term><term>Uidity</term><term>Uorescence polarization</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Lapin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The study aims at elucidating the mechanism involved in the cell dysfunction or impairment and the protective effects of phospholipase A2 (PLA2) inhibitors in endotoxin shock. Thirty-four rabbits were divided randomly into four groups: (1) normal control group (NC, n=6), receiving saline intravenously; (2) endotoxin shock group (ES, n=12), receiving 3mg/kg of E. coli endotoxin; (3) chloroquine pretreated group (CQ, n=8), receiving 3mg/kg of chloroquine 3min before endotoxin injection and (4) chlorpromazine pretreated group (CPZ, n=8), receiving 0.3mg/kg of chlorpromazine 30min before endotoxin injection. Hepatic mitochondria were extracted either 8h after commencement of the experiment or when the animals died for detecting PLA2 activity, membrane fluidity, membrane bound succinate dehydrogenate (SDH) and malondialdehyde (MDA). Mitochondria of the lung, heart and kidney were also used for detection of the membrane fluidity. It was revealed that the survival rate of 8h was 100% (NC), 58% (ES), 87.5% (CQ) and 75% (CPZ), respectively. Mean arterial pressure (MAP) dropped soon after endotoxin injection and descended continuously afterwards in the ES group (P<0.01). Fluorescence polarization, microviscosity and anisotrophy with a DPH probe were elevated above control levels (P<0.01). SDH was decreased obviously following endotoxin infusion (P<0.01). Chloroquine and chlorpromazine, serving as PLA2 inhibitors, could abate cellular dysfunction and increase survival rate. It is proposed that PLA2 plays a pivotal role in cellular injury in endotoxin shock. PLA2 inhibitor might serve as a useful adjunct in combating sepsis and shock.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Song, S M" sort="Song, S M" uniqKey="Song S" first="S. M" last="Song">S. M Song</name></noRegion><name sortKey="Guo, S Q" sort="Guo, S Q" uniqKey="Guo S" first="S. Q" last="Guo">S. Q Guo</name><name sortKey="Li, Z" sort="Li, Z" uniqKey="Li Z" first="Z" last="Li">Z. Li</name><name sortKey="Liu, J C" sort="Liu, J C" uniqKey="Liu J" first="J. C" last="Liu">J. C Liu</name><name sortKey="Lu, S M" sort="Lu, S M" uniqKey="Lu S" first="S. M" last="Lu">S. M Lu</name><name sortKey="Wang, Z G" sort="Wang, Z G" uniqKey="Wang Z" first="Z. G" last="Wang">Z. G Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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