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Página 1 a partir de 165 resultados
Suppressive effect of caffeine on hepatitis and apoptosis induced by tumor necrosis factor-alpha, but not by the anti-Fas antibody, in mice.
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Tumor necrosis factor (TNF)-alpha-induced hepatitis and apoptosis, as respectively assessed by serum enzyme activities and hepatic DNA fragmentation were effectively suppressed by a single force-feeding of caffeine (100 mg/kg) 1.5 h before injecting the drug. In contrast, caffeine had no significant
Effect of Caffeine on Serum Tumour Necrosis Factor Alpha and Lactate Dehydrogenase in Wistar Rats Exposed to Cerebral Ischaemia-reperfusion Injury.
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Caffeine is known to confer neuro-protection via A1 and A2A adenosine receptor antagonism in which adenosine neuro-modulates excitotoxic release of glutamate. Currently, it is unclear whether caffeine modulates inflammation in ischaemic stroke model. The present study examined effects of caffeine
Caffeine protects human skin fibroblasts from acute reactive oxygen species-induced necrosis.
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Oxidative damage by reactive oxygen species (ROS) plays a major role in aging and carcinogenesis. Little is known about either the effects of acute ROS in necrosis and inflammation of skin or the therapeutic agents for prevention and treatment. Previously, our laboratory identified caffeine as an
Acute hemorrhagic myocardial necrosis and sudden death of rats exposed to a combination of ephedrine and caffeine.
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Because of possible side effects of herbal medicines containing ephedrine and guarana-derived caffeine, including increased risk of stroke, myocardial infarction, and sudden death, the Food and Drug Administration recently banned the sale of ephedra-containing products, specifically over-the-counter
Caffeine potentiates the lethality of tumour necrosis factor in cancer cells.
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In this study we have investigated the interaction of caffeine, a prototypic methylxanthine, and TNF on the induction of cell death in mouse and human cell lines during progression from G1 to successive phases of the cell cycle. Exposure of cells to TNF (0.1-100 ng ml-1) as single agent for 48 h
EVALUATION OF CAFFEINE AND OUABAIN AS PERMISSIVE AGENTS IN THE PRODUCTION OF MYOCARDIAL NECROSIS.
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Factors Associated with Higher Pro-Inflammatory Tumor Necrosis Factor-α Levels in Young Women with Type 1 Diabetes.
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OBJECTIVE
While cytokines play a role in the etiology of type 1 diabetes, cytokines later in the disease are less understood. We therefore investigated associations of pro-inflammatory tumor necrosis factor-α levels measured at prolonged disease duration with C-peptide at diagnosis, long-term
Caffeine-assisted chemotherapy and minimized tumor excision for nonmetastatic osteosarcoma.
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Osteosarcoma is usually treated with intensive preoperative and postoperative chemotherapy and wide tumor resection, resulting in a 60% to 70% 5-year survival rate. Caffeine has a DNA-repair inhibiting effect. We therefore investigated the impact of caffeine given in conjunction with chemotherapy
Increased hepatotoxicity of acetaminophen by concomitant administration of caffeine in the rat.
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Since caffeine is frequently co-administered with acetaminophen, it is of clinical interest to study the effect of caffeine on the hepatotoxicity of acetaminophen. In male Sprague-Dawley rats fasted for 18 h, concomitant administration of caffeine (0.1 g/kg, i.p.) as judged by increased serum enzyme
The induction of renal papillary necrosis in Gunn rats by analgesics and analgesic mixtures.
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Homozygous members of the mutant Gunn strain of Wistar rats genetically lack the enzyme uridine diphosphate glucuronyl transferase. "High" and "low" dose gavage feeding for 18-34 days of an analgesic mixture containing aspirin, phenacetin and caffeine (APC) confirmed the previously reported
[Digital necrosis in hand by uncommon mechanism].
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A 43-year-old, non-smoking man presented with acute ischemic lesions of his left hand. He had been taking beta-blockers for his arterial hypertension. The day before the occurrence of these acute lesions, he self medicated with a drug containing ergotamine and caffeine because of a headache. About
Phenolic compounds isolated from Dioscorea zingiberensis protect against pancreatic acinar cells necrosis induced by sodium taurocholate.
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One new bibenzyl (1) and one new phenanthrene (2), together with two known bibenzyls (3-4) and four known diarylheptanoids (5-8) were isolated from the rhizomes of Dioscorea zingiberensis. The structures of 1-2 were elucidated by spectroscopic methods including 1D and 2D NMR. Phenols 1-8 were
Caffeine metabolites are inhibitors of the nuclear enzyme poly(ADP-ribose)polymerase-1 at physiological concentrations.
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The activity of the nuclear enzyme poly(ADP-ribose)polymerase-1 (E.C.2.4.2.30), which is highly activated by DNA strand breaks, is associated with the pathophysiology of both acute as well as chronic inflammatory diseases. PARP-1 overactivation and the subsequent extensive turnover of its substrate
Acetaminophen-induced hepatotoxicity: antagonistic action of caffeine in mice.
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Studies of interactions in mice between acetaminophen (ACM) and caffeine (CAF) revealed that CAF given immediately after ACM antagonized the acute toxicity of ACM and reduced the severity of ACM-induced hepatic necrosis as assessed grossly and microscopically. It also attenuated the elevations of
Papillary necrosis in experimental analgesic nephropathy.
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A proprietary aspirin, phenacetin, and caffeine preparation given to rats in a dose equivalent to that taken by patients with analgesic nephropathy produced papillary necrosis in 55%. There was a higher incidence in rats deprived of fluids overnight.Papillary necrosis was not noted in rats receiving
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