lysophosphatidylethanolamine/inflammatie

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2-Polyunsaturated acyl lysophosphatidylethanolamine attenuates inflammatory response in zymosan A-induced peritonitis in mice.

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In the present study, the anti-inflammatory action of lysophosphatidylethanolamine (lysoPtdEtn), orally administered, in zymosan A-induced peritonitis was examined. Oral administration of 2-DHA-lysoPtdEtn (ED(50), ~111 μg/kg) or 2-ARA-lysoPtdEtn (ED(50), 221 μg/kg) was found to inhibit the plasma

Systems wide analyses of lipids in the brainstem during inflammatory orofacial pain - evidence of increased phospholipase A(2) activity.

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Recent studies suggest that CNS phospholipase A(2) (PLA(2) ) isoforms play a role in nociception, but until now, direct evidence of increased brain PLA(2) activity during allodynia or hyperalgesia is lacking. The present study was carried out, using lipidomics or systems wide analyses of lipids

Phospholipids in inflammatory synovial effusions.

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The concentration of phospholipids and proteins was determined in 23 inflammatory synovial fluids obtained from human knee joints. The synovial fluid to plasma phospholipid ratio (0.48 and 0.37 at high and low inflammatory state) was lower than the value found for the total protein content (0.68 and

Inverse Phosphatidylcholine/Phosphatidylinositol Levels as Peripheral Biomarkers and Phosphatidylcholine/Lysophosphatidylethanolamine-Phosphatidylserine as Hippocampal Indicator of Postischemic Cognitive Impairment in Rats.

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Vascular dementia is a transversal phenomenon in different kinds of neurodegenerative diseases involving acute and chronic brain alterations. Specifically, the role of phospholipids in the pathogenesis of dementia remains unknown. In the present study, we explored phospholipid profiles a month

PM2.5-induced inflammation and lipidome alteration associated with the development of atherosclerosis based on a targeted lipidomic analysis.

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Epidemiological studies have confirmed that PM_2.5 could contribute to the development of atherosclerosis accompanied with lipids dysregulation. However, the lipids biomarkers involved in this progress remain largely unknown. In this study, a targeted lipidomic approach was used to find

Serum lipidomic analysis from mixed neutron/X-ray radiation fields reveals a hyperlipidemic and pro-inflammatory phenotype.

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Heightened threats for nuclear terrorism using improvised nuclear devices (IND) necessitate the development of biodosimetry assays that could rapidly assess thousands of individuals. However, the radiation exposures from an IND may be complex due to mixed fields of neutrons and photons (γ-rays),

C-reactive protein specifically enhances platelet-activating factor-induced inflammatory activity in vivo.

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Platelet-activating factor (PAF) is a potent lipid mediator that is implicated in numerous inflammatory diseases. C-reactive protein (CRP) is an acute-phase plasma protein that increases rapidly and dramatically in response to inflammation. In this study, we investigated the effect of the

Relationship between the lipidome, inflammatory markers and insulin resistance.

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The objectives of the present study were to (1) examine the effects of the phenotypic factors age, gender and BMI on the lipidomic profile and (2) investigate the relationship between the lipidome, inflammatory markers and insulin resistance. Specific ceramide, phosphatidylcholine and

The association of specific metabolites of lipid metabolism with markers of oxidative stress, inflammation and arterial stiffness in men with newly diagnosed type 2 diabetes.

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OBJECTIVE To determine whether circulating metabolic intermediates are associated with inflammation, oxidative stress and arterial stiffness in men with newly diagnosed type 2 diabetes and investigate the circulating metabolic intermediates that may predict the risk of developing

Isolation and characterization of a phospholipase A2 from an inflammatory exudate.

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Sterile peritoneal exudates produced in rabbits injected with 1% glycogen contain a phospholipase A activity in a cell-free supernatant fraction that hydrolyzed a synthetic phospholipid (1,2-diacyl-sn-glycero-3-phospho-ethanolamine) and phospholipids of autoclaved Escherichia coli. This

Lysophosphatidylethanolamine is - in contrast to - choline - generated under in vivo conditions exclusively by phospholipase A2 but not by hypochlorous acid.

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Inflammatory liver diseases are associated with oxidative stress mediated particularly by neutrophilic granulocytes. At inflammatory loci, hypochlorous acid (HOCl) is generated by myeloperoxidase. HOCl reacts with a large variety of molecules and induces (among other reactions) the formation of

[Semi-synthesis and proposed structure of platelet-activating factor (P.A.F.): PAF-acether an alkyl ether analog of lysophosphatidylcholine].

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We have studied the molecular structure of platelet-activating factor" (P.A.F.), a mediator of inflammation obtained from blood leukocytes, macrophages, and platelets themselves. We have semi-synthetized a substance that possesses all the known physicochemical and biological characteristics of

Common disbalance in the brain parenchyma of dementias: Phospholipid profile analysis between CADASIL and sporadic Alzheimer's disease.

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Sporadic Alzheimer's disease (SAD) is the most common form of dementia, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most frequent hereditary ischemic small vessel disease of the brain. Relevant biomarkers or specific metabolic

Hepatotoxic effects of inhalation exposure to polycyclic aromatic hydrocarbons on lipid metabolism of C57BL/6 mice.

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Inhalation from ambient air and cigarette smoke is a common route of human exposure to polycyclic aromatic hydrocarbons (PAHs). Little information is available regarding hepatotoxicities of inhaled PAHs so for. In this study, we evaluated the toxic effects of intratracheally instilled benzo[a]pyrene

cPLA2 and desaturases underlie the tau hyperphosphorylation offset induced by BACE knock-down in neuronal primary cultures.

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Inflammation has been suggested to play early and perhaps causative roles in Alzheimer's disease (AD) pathogenesis possibly in part by the overactivation of the aspartic acid protease named β-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1), which is responsible for the β-amyloid

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