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lysophosphatidylcholine/nekrose

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Alteration of membrane phospholipid fatty acid compositions has been shown to be important for leukocyte inflammatory responses. Such modification of the molecular species of these lipid classes requires deacylation and reacylation reactions and for phosphatidylcholines, lysophosphatidylcholine

Inflammatory stress increases receptor for lysophosphatidylcholine in human microvascular endothelial cells.

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The atherogenic serum lysophosphatidylcholine (LPC) is known to mediate vascular endothelial responses ranging from upregulation of adhesion molecules and growth factors to secretion of chemokines and superoxide anion. We investigated whether endothelial cells express receptors for LPC, which may

Lysophosphatidylcholine induces apoptosis in AR42J cells.

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Phospholipase A2 (PLA2) has been suggested to play an important role in the pathogenesis of acute pancreatitis, in part through the PLA2-generated phospholipid by-products, most notably lysophosphatidylcholine (lyso-PC). The effects of lyso-PC on pancreatic acinar cells, other than the induction of

Lyso-phosphatidylcholine is implicated in thioacetamide-induced liver necrosis.

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Thioacetamide is a weak hepatocarcinogen. To determine whether alterations in lysophosphatidylcholine are implicated in thioacetamide-induced hepatic necrosis, rats were injected i.p. with this agent (50 mg/Kg body weight per day) or diluent for 1, 3, 8 and 30 days. Serum catalytic activities of

Tumor necrosis factor cytotoxicity is associated with phospholipase D activation.

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The activation of phospholipase D in different cell lines treated with recombinant human tumor necrosis factor (TNF) has been investigated. When the murine fibrosarcoma cell lines L929 and WEHI164c113, as well as the human promonocytic cell line U937, were prelabeled with [14C]palmitic acid or

[Effect of phospholipase A2 on pancreatic parenchymal necrosis in acute pancreatitis in rats].

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The effect and mechanism of phospholipase A2 (PLA2) on pancreatic parenchymal necrosis in acute pancreatitis (AP) in rats were studied. Normal saline (NS), PLA2, phosphatidylcholine (PC), and PLA2 mixed PC were respectively injected into the biliopancreatic duct of the rat. The mixture of PLA2 and

Lysophosphatidylcholine activates transcription factor NF-kappaB and AP-1 in AR42J cells.

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Phospholipase A2 (PLA2) has been suggested in the pathogenesis of acute pancreatitis, in part through the PLA2-generated phospholipid by-products, most notably lysophosphatidylcholine (lyso-PC). The effects of lyso-PC on pancreatic acinar cells other than necrosis are poorly characterized. Recent

Tumor necrosis factor induces rapid production of 1'2'diacylglycerol by a phosphatidylcholine-specific phospholipase C.

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Tumor necrosis factor (TNF) is a proinflammatory polypeptide that is able to induce a great diversity of cellular responses via modulating the expression of a number of different genes. One major pathway by which TNF receptors communicate signals from the membrane to the cell nucleus involves

Acylation of lysophosphatidylcholine plays a key role in the response of monocytes to lipopolysaccharide.

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Mononuclear phagocytes play a pivotal role in the progression of septic shock by producing tumor necrosis factor-alpha (TNF-alpha) and other inflammatory mediators in response to lipopolysaccharide (LPS) from Gram-negative bacteria. Our previous studies have shown monocyte and macrophage activation
The cytotoxic mechanism of recombinant human tumor necrosis factor (TNF) in human osteosarcoma cells (TE85) was studied from the point of view of phospholipid metabolism. The TNF-induced cytotoxicity, determined by using the dye uptake method, was dose-dependent in the range of 100-10,000 U/ml.
OBJECTIVE To examine the effect of tumor necrosis factor-alpha (TNF-alpha) on pulmonary artery pressure and on total protein, phospholipid, lysophosphatidylcholine, phosphatidylcholine, phosphatidylinositol, and phosphatidylglycerol content in the bronchoalveolar lavage-accessible space of the

Resveratrol alleviates lysophosphatidylcholine-induced damage and inflammation in vascular endothelial cells.

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The role of resveratrol (trans-3,5,4'-trihydroxystilbene; RES) in lysophosphatidylcholine (LPC)‑induced injury and inflammation in endothelial cells (regarded as an early event in arteriosclerosis) is unclear. The present study investigated whether RES reduces lactate dehydrogenase (LDH) activity
Microalgae have been shown to be excellent producers of lipids, pigments, carbohydrates, and a plethora of secondary metabolites with possible applications in the pharmacological, nutraceutical, and cosmeceutical sectors. Recently, various microalgal raw extracts have been found to have
Lysophosphatidylcholines (lysoPCs) have been known to be bioactive lipid mediators, which take part in various biological and pathological processes. In the present study, we examined the anti-inflammatory actions of 2-docosahexaenoyl lysophosphatidylcholine (2-docosahexaenoyl-lysoPC) in vitro as

Therapeutic efficacy of lysophosphatidylcholine in severe infections caused by Acinetobacter baumannii.

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Due to the significant increase in antimicrobial resistance of Acinetobacter baumannii, immune system stimulation to block infection progression may be a therapeutic adjuvant to antimicrobial treatment. Lysophosphatidylcholine (LPC), a major component of phospholipids in eukaryotic cells, is
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