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lysolecithin/воспаление
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Lysolecithin-mediated inflammatory reaction in rabbit gallbladder. Permeability increase and enzyme liberation.
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Aseptic inflammation in the gallbladder wall was studied in vitro using rabbit gallbladders. Wall permeability changes, measured as changes in the transmural passage of radioactively labelled hippuran and biligraphin as well as enzyme (acid phosphatase) release from wall to lumen were registered as
Effect of leukocyte hydrolases on bacteria. XIII. Role played by leukocyte extracts, lysolecithin, phospholipase a2, lysozyme, cationic proteins, and detergents in the solubilization of lipids from Staphylococcus aureus and group A streptococci: relation to bactericidal and bacteriolytic reactions in inflammatory sites.
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The bactericidal and bacteriolytic effects of lysolecithin (LL) and egg-white lysozyme (LYZ) on Staph. aureus and group A streptococci and the solubilization of phospholipids from the bacterial membranes by these agents was studied. Low concentrations of lysolecithin (1--10 microgrames/ml) are
Inflammatory changes in newly formed vessels of carrageenin-induced granulomas after systemic 5-hydroxytryptamine, bradykinin, kallikrein, or lysolecithin.
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Inflammatory changes in tumour vessels after systemic 5-hydroxytryptamine, bradykinin, kallikrein, or lysolecithin.
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Some effects of lysolecithin in vivo and in vitro and their possible relations to the inflammatory process.
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The effect of lysolecithin on prostanoid and platelet-activating factor formation by human gall-bladder mucosal cells.
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It has been demonstrated that lysolecithin (lysophosphatidyl choline, LPC) produces experimental cholecystitis in cats mediated by arachidonic acid metabolites. LPC is a cytolytic agent that has been postulated as a contributing factor in the development of cholecystitis in humans. The purpose of
Complement potentiates the degradation of myelin proteins by plasmin: implications for a mechanism of inflammatory demyelination.
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A previous finding, that the basic protein in lyophilized bovine myelin was degraded by macrophage-conditioned media in the presence of plasminogen, suggested that the macrophage-secreted plasminogen activator, along with plasminogen, might have a role in destruction of myelin during inflammatory
The biochemical prerequisites for preventing pathogenic lysolecithin activity in the human gallbladder.
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Human gallbladder epithelium was disintegrated to complete loss of microscopic structure and incubated at 37 degree C together with unlabelled lysolecithin and 14C-lysolecithin. During each incubation lysolecithin was degraded and stoichiometrically equivalent amounts of free fatty acids formed. The
Formation and inhibition of lysolecithin in human gallbladder bile.
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Homogenized human gallbladder epithelium was incubated at 37 degrees C with 14C-lecithin in diluted gallbladder bile. During the incubation, lecithin was transformed to lysolecithin. The reaction rate was higher at pH 4.5 than at pH 7.0. No degradation of lecithin occurred if the reaction mixture
Vasodepression ex vivo after administration of inflammatory mediators in vivo in the rat.
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When rats were pretreated by intraplantar or i.v. injection of various inflammatory mediators, the vasopressor effect of i.a. norepinephrine in the subsequently isolated perfused hindlegs of the rats was found to be partly depressed. This vasodepression could also be detected if mediators were
The inflammatory effects of crystalline cholesterol monohydrate in the guinea pig gallbladder in vivo.
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BACKGROUND
The etiologic role of crystalline material in inflammatory arthritis is well established. The role of crystals in cholecystitis is unclear. We hypothesized that crystalline cholesterol monohydrate stimulates guinea pig gallbladder inflammation in vivo.
METHODS
Crystalline cholesterol
The prerequisites for local lysolecithin formation in the human gallbladder.
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Human gallbladder epithelium was disintegrated to complete loss of microscopic structure. The material obtained - an extract - was incubated at 37 degrees C together with a mixture of lecithin and lysolecithin, phospholipids known to be present in bile. During such incubation a change in the
Human antibodies accelerate the rate of remyelination following lysolecithin-induced demyelination in mice.
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Immunoglobulin-based therapies are becoming increasingly common for the treatment of neurologic and autoimmune diseases in humans. In this study, we demonstrate that systemic administration of either polyclonal human immunoglobulins or specific human monoclonal antibodies can accelerate the rate of
Apolipoprotein E Mimetic Promotes Functional and Histological Recovery in Lysolecithin-Induced Spinal Cord Demyelination in Mice.
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OBJECTIVE
Considering demyelination is the pathological hallmark of multiple sclerosis (MS), reducing demyelination and/or promoting remyelination is a practical therapeutic strategy to improve functional recovery for MS. An apolipoprotein E (apoE)-mimetic peptide COG112 has previously demonstrated
Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin.
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Multiple sclerosis (MS) is a chronic autoimmune, inflammatory disease in the central nervous system (CNS) characterized by loss of oligodendrocytes, myelin axons, and neurons. Remyelination is an endogenous repair mechanism, which recovers the loss of myelin and is able to preserve functional axons.
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