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methyl palmitate/nekróza
Odkaz sa uloží do schránky
14 výsledky
Effects of methyl palmitate on cytokine release, liver injury and survival in mice with sepsis.
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The effects of methyl palmitate (MP), a known inhibitor of Kupffer cells, were studied in a model of polymicrobial sepsis induced in CD-1 mice by cecal ligation and puncture (CLP). The inhibition of Kupffer cells by pretreatment with MP was shown by the reduced phagocytosis, the production of tumor
Experimental elimination of the splenic function by ethyl and methyl palmitate and significance of these substances from an immunological point of view.
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Our experiments with rats dealt with finding a possible functional splenic elimination by using an i.v. injection of ethyl and methyl palmitate emulsion. Simultaneously, immunological effects were determined in both substances. After applying ethyl palmitate an extensive splenic necrosis could be
Cytoprotective potential of tiron and methyl palmitate against acetaminophen-induced acute liver injury.
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Acute liver injury is a debilitating disorder associated with loss of synthetic and detoxifying functions of the liver. This investigation was designed to assess cytoprotective efficacy of daily oral tiron (300 mg/kg) and daily oral methyl palmitate (300 mg/kg) against acetaminophen-induced acute
Anti-inflammatory activity of methyl palmitate and ethyl palmitate in different experimental rat models.
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Methyl palmitate (MP) and ethyl palmitate (EP) are naturally occurring fatty acid esters reported as inflammatory cell inhibitors. In the current study, the potential anti-inflammatory activity of MP and EP was evaluated in different experimental rat models. Results showed that MP and EP caused
Methyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophages.
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Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential
Protective effects of methyl palmitate against silica-induced pulmonary fibrosis in rats.
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Silicosis is one of the most prevalent chronic occupational pulmonary diseases worldwide. The present study aimed to investigate the effects of methyl palmitate on silica-induced lung fibrosis in rats and explore the possible mechanisms. Male Sprague-Dawley rats were divided into 3 groups: group I
Targeting MAPKs, NF-κB, and PI3K/AKT pathways by methyl palmitate ameliorates ethanol-induced gastric mucosal injury in rats.
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Excessive drinking of alcohol has been frequently associated with gastric injury; however, its underlying molecular mechanisms have been inadequately investigated. Methyl palmitate (MP) has demonstrated marked hepato-, cardio- and pulmonary protective features; however, its effects on
Influence of a reticuloendothelial-suppressing agent on liver tumor growth in the rat.
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Reticuloendothelial (RE) function was evaluated by measuring the biokinetics of a standardized 99Tcm-sulphur colloid. Methyl palmitate was administered intravenously on two consecutive days. A statistically significant reduction in the colloid uptake rate of the liver was registered after methyl
Antileukemic effects of Didemnum psammatodes (Tunicata: Ascidiacea) constituents.
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Chemical investigation of the methanolic extract of the ascidian Didemnum psammatodes has led to the identification of fourteen known compounds: three methyl esters (methyl myristate, methyl palmitate and methyl stearate), four steroids (cholesterol, campesterol, stigmasterol and beta-sitosterol),
Kupffer cells are causally responsible for the mitogenic effect of peroxisome proliferators.
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WY-14,643 [4-chloro-6-(2,3-xylidino)pyrimidinylthio-acetic acid] is a well-known non-genotoxic carcinogen and peroxisome proliferator that causes liver cancer in rodents by unknown mechanisms. Its ability to sustain elevated rates of hepatocyte DNA synthesis is most likely pivotal in the ultimate
Relation of the reticuloendothelial function to endotoxin hepatotoxicity.
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The present study was undertaken in rats to clarify whether endotoxin hepatotoxicity can be modified by phagocytic activity of the reticuloendothelial system. Pretreatment with cortisone acetate, diethylstilbestrol, methyl palmitate, triolein or gadolinium chloride markedly improved the mortality
Single chain antibodies specific for fatty acids derived from a semi-synthetic phage display library.
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The biological activities of many acylated molecules are lipid dependent. Lipids, however, are poorly immunogenic or non-immunogenic. We employed a phage display semi-synthetic human antibody library to isolate anti-lipid antibodies. Selection was done against methyl palmitate, a 16 carbon aliphatic
Modification of galactosamine-induced liver injury in rats by reticuloendothelial system stimulation or depression.
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The reticuloendothelial system has been implicated in galactosamine-induced liver injury because of a correlation between phagocytic alterations induced by colloidal carbon or endotoxin, and development of liver necrosis. To evaluate this concept, the influence of galactosamine on liver function and
Perivascular adipose tissue, vascular reactivity and hypertension.
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Most blood vessels are surrounded by a variable amount of adventitial adipose tissue, perivascular adipose tissue (PVAT), which was originally thought to provide mechanical support for the vessel. It is now known that PVAT secretes a number of bioactive substances including vascular endothelial
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