FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2401389920> ?p ?o ?g. }

• W2401389920 endingPage "628" @default.
• W2401389920 startingPage "617" @default.
• W2401389920 abstract "In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. Interleukin-1㄁ (IL-1, 50 ㄍg/rat) was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin F2㄁ (6-keto-PGF2㄁) was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier." @default.
• W2401389920 created "2016-06-24" @default.
• W2401389920 creator A5009541722 @default.
• W2401389920 creator A5013875310 @default.
• W2401389920 creator A5049903270 @default.
• W2401389920 creator A5050953995 @default.
• W2401389920 creator A5062491145 @default.
• W2401389920 creator A5065400036 @default.
• W2401389920 creator A5069938285 @default.
• W2401389920 date "1998-01-01" @default.
• W2401389920 modified "2023-09-23" @default.
• W2401389920 title "Effect of the Inhibition of PLA2 on Oxidative Lung Injury Induced by $Interleukin-1{alpha}$" @default.
• W2401389920 hasPublicationYear "1998" @default.
• W2401389920 type Work @default.
• W2401389920 sameAs 2401389920 @default.
• W2401389920 citedByCount "0" @default.
• W2401389920 crossrefType "journal-article" @default.
• W2401389920 hasAuthorship W2401389920A5009541722 @default.
• W2401389920 hasAuthorship W2401389920A5013875310 @default.
• W2401389920 hasAuthorship W2401389920A5049903270 @default.
• W2401389920 hasAuthorship W2401389920A5050953995 @default.
• W2401389920 hasAuthorship W2401389920A5062491145 @default.
• W2401389920 hasAuthorship W2401389920A5065400036 @default.
• W2401389920 hasAuthorship W2401389920A5069938285 @default.
• W2401389920 hasConcept C126322002 @default.
• W2401389920 hasConcept C134018914 @default.
• W2401389920 hasConcept C141983124 @default.
• W2401389920 hasConcept C145156650 @default.
• W2401389920 hasConcept C181199279 @default.
• W2401389920 hasConcept C185592680 @default.
• W2401389920 hasConcept C203014093 @default.
• W2401389920 hasConcept C2776151105 @default.
• W2401389920 hasConcept C2776348555 @default.
• W2401389920 hasConcept C2776551241 @default.
• W2401389920 hasConcept C2776685179 @default.
• W2401389920 hasConcept C2776914184 @default.
• W2401389920 hasConcept C2777714996 @default.
• W2401389920 hasConcept C2777961210 @default.
• W2401389920 hasConcept C2778048844 @default.
• W2401389920 hasConcept C2779291727 @default.
• W2401389920 hasConcept C42219234 @default.
• W2401389920 hasConcept C55493867 @default.
• W2401389920 hasConcept C71924100 @default.
• W2401389920 hasConcept C98274493 @default.
• W2401389920 hasConcept C99971728 @default.
• W2401389920 hasConceptScore W2401389920C126322002 @default.
• W2401389920 hasConceptScore W2401389920C134018914 @default.
• W2401389920 hasConceptScore W2401389920C141983124 @default.
• W2401389920 hasConceptScore W2401389920C145156650 @default.
• W2401389920 hasConceptScore W2401389920C181199279 @default.
• W2401389920 hasConceptScore W2401389920C185592680 @default.
• W2401389920 hasConceptScore W2401389920C203014093 @default.
• W2401389920 hasConceptScore W2401389920C2776151105 @default.
• W2401389920 hasConceptScore W2401389920C2776348555 @default.
• W2401389920 hasConceptScore W2401389920C2776551241 @default.
• W2401389920 hasConceptScore W2401389920C2776685179 @default.
• W2401389920 hasConceptScore W2401389920C2776914184 @default.
• W2401389920 hasConceptScore W2401389920C2777714996 @default.
• W2401389920 hasConceptScore W2401389920C2777961210 @default.
• W2401389920 hasConceptScore W2401389920C2778048844 @default.
• W2401389920 hasConceptScore W2401389920C2779291727 @default.
• W2401389920 hasConceptScore W2401389920C42219234 @default.
• W2401389920 hasConceptScore W2401389920C55493867 @default.
• W2401389920 hasConceptScore W2401389920C71924100 @default.
• W2401389920 hasConceptScore W2401389920C98274493 @default.
• W2401389920 hasConceptScore W2401389920C99971728 @default.
• W2401389920 hasIssue "5" @default.
• W2401389920 hasLocation W24013899201 @default.
• W2401389920 hasOpenAccess W2401389920 @default.
• W2401389920 hasPrimaryLocation W24013899201 @default.
• W2401389920 hasRelatedWork W154867420 @default.
• W2401389920 hasRelatedWork W1772053531 @default.
• W2401389920 hasRelatedWork W1964129681 @default.
• W2401389920 hasRelatedWork W1981820264 @default.
• W2401389920 hasRelatedWork W2045018547 @default.
• W2401389920 hasRelatedWork W2070743437 @default.
• W2401389920 hasRelatedWork W2089560740 @default.
• W2401389920 hasRelatedWork W2106725146 @default.
• W2401389920 hasRelatedWork W2117737600 @default.
• W2401389920 hasRelatedWork W2126330629 @default.
• W2401389920 hasRelatedWork W2135371537 @default.
• W2401389920 hasRelatedWork W2135637410 @default.
• W2401389920 hasRelatedWork W2142420977 @default.
• W2401389920 hasRelatedWork W2151556390 @default.
• W2401389920 hasRelatedWork W2291953636 @default.
• W2401389920 hasRelatedWork W2301108870 @default.
• W2401389920 hasRelatedWork W2319272871 @default.
• W2401389920 hasRelatedWork W2367613590 @default.
• W2401389920 hasRelatedWork W3192632943 @default.
• W2401389920 hasRelatedWork W2326106982 @default.
• W2401389920 hasVolume "2" @default.
• W2401389920 isParatext "false" @default.
• W2401389920 isRetracted "false" @default.
• W2401389920 magId "2401389920" @default.
• W2401389920 workType "article" @default.