lysolecithin/necrosis

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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

Experimental pancreatitis in the rat. Light and electron microscopical observations on early pancreatic lesions induced by intraductal injection of trypsin, phospholipase A2, lysolecithin and non-ionic detergent.

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Trypsin, phospholipase A2, lysolecithin or non-ionic detergent polyoxyethylene p-t-octyl phenol solutions were injected into the rat biliopancreatic duct. Histological and ultrastructural changes in the gland were studied 15 min and 3 h after the injections. The rough surfaced endoplasmic reticulum

Role of various phospholipases A2 and inhibitors in the pathogenesis and prevention of pancreatic acinar cell necrosis: studies with isolated rat pancreatic acini.

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BACKGROUND Phospholipase A2 (PLA2) may play a central role in the pathogenesis of pancreatic acinar cell necrosis. Several questions, however, are unsolved: Is acinar cell necrosis caused by PLA2 derived from infiltrating leukocytes or from pancreatic PLA2 itself? Does PLA2 cause cellular lysis by

Evaluation of Myelin Radiotracers in the Lysolecithin Rat Model of Focal Demyelination: Beware of Pitfalls!

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The observation that amyloid radiotracers developed for Alzheimer's disease bind to cerebral white matter paved the road to nuclear imaging of myelin in multiple sclerosis. The lysolecithin (lysophosphatidylcholine (LPC)) rat model of demyelination proved useful in evaluating and comparing candidate

[Acute necrotizing pancreatitis caused by the injection of lysolecithin into the pancreatic duct in the rat. Its natural course and effect of drugs on rate of survival].

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Acute experimental pancreatitis was induced by retrograde injection of 0.15 ml of 0.8% lysolecithin into the pancreatic duct of Wistar rats. This procedure was always followed by severe necrosis of pancreatic parenchyma, bloody ascites and numerous fat necroses in the abdominal cavity.

[Pathophysiology of acute pancreatitis].

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Recent experiments in different animal models of acute pancreatitis have improved our understanding of the pathophysiology of this disease. The present review discusses the individual steps and mechanisms and puts them into a pathophysiologic concept for the two most important forms of acute

Role of phospholipase A2 in pancreatic acinar cell damage and possibilities of inhibition: studies with isolated rat pancreatic acini.

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Phospholipase A2 (PLA2) has been postulated to play an important role in the pathogenesis of acute pancreatitis. To study the mechanism through which PLA2 may cause cellular damage, we used an in vitro model of isolated rat pancreatic acini prepared by collagenase digestion. Newly synthesized

The multimolecular cascade of spinal cord injury. Studies on prostanoids, calcium, and proteinases.

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Experimental spinal cord injury in animals induced by weight drop produces neurological deficit and paralysis. Correlation of the progressive morphological changes in the lesion by both light and electron microscopy with the biochemical alterations revealed ischemia, edema, hemorrhage, tissue

Investigations into various pancreatic enzymes.

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The effects of several pancreatic enzymes on living tissue incapable of autodigestion were studied to analyse elements of the "pluralistic events of acute hemorrhagic pancreatitis" (Becker 1981). Phospholipase A2 induces (via toxic lysolecithin) cytotoxic necrosis in the testis; elastase (via

Effect of long-term ethanol feeding on the restoration process of acute necrotizing pancreatitis induced in rats.

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This study was conducted to elucidate the possible influence of long-term peroral administration of alcohol on the repair process of acute necrotizing pancreatitis. Male Wistar rats fed with balanced diet were divided into two groups. The first group had free access to 15% ethanol, and the second

Surfen, a proteoglycan binding agent, reduces inflammation but inhibits remyelination in murine models of Multiple Sclerosis.

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Proteoglycans are promising therapeutic targets in Multiple Sclerosis (MS), because they regulate many aspects of the immune response. This was studied using surfen, an agent that binds both heparan sulphate proteoglycans (HSPGs) and chondroitin sulphate proteoglycans (CSPGs). Initial cell culture

Comparison of different treatment modalities in experimental pancreatitis in rats.

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Lipolytic enzymes may play a role in the pathogenesis of acute pancreatitis. Therefore, the effects of a lipase inhibitor, THL (tetrahydrolipstatin), a protease inhibitor, FUT (nafamostat mesilate), and albumin under different conditions in rats were investigated. (a) Isolated pancreatic acini were

Glucagon treatment of experimental acute pancreatitis.

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CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals

Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces mononuclear leukocyte adhesion molecules in cultured human and rabbit arterial endothelial cells.

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Accumulation of monocyte-derived foam cells in focal areas of the arterial intima is one of the key events in early atherogenesis. We have examined the effect of lysophosphatidylcholine (lyso-PC; lysolecithin), a major phospholipid component of atherogenic lipoproteins, on the expression of adhesion

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