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tocopherol/nekrosis
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Alpha tocopherol decreases lipid peroxidation, neuronal necrosis, and reactive gliosis in reaggregate cultures of fetal rat brain.
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This study explored the effects of the lipid-soluble free radical scavenger, alpha tocopherol (vitamin E), on neuronal injury and glial protein accumulation in a well-characterized, three-dimensional, mixed neuronal and glial culture system derived from fetal rat prosencephalon. As these
[Effect of alpha-tocopherol on apoptosis and necrosis of rat thymocytes induced by calcium ionophore A23187 in various concentrations].
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It has been established that alpha-tocopherol prevented rat thymocytes apoptotic death induced by low concentration (250 nM) of calcium ionophore A23187. When necrotic cell death was induced high concentration (10 microM) of calcium ionophore A23187 alpha-tocopherol was able to alter necrosis to
Cytoprotective effect of γ-tocopherol against tumor necrosis factor α induced cell dysfunction in L929 cells.
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The antioxidant vitamin γ-tocopherol exerts protective and anti-inflammatory effects in various models of critical illness. The combination of actinomycin D and tumor necrosis factor α (TNFα) in the immortalized fibroblast cell line L929 is a well-established method to model pro-inflammatory
Effect of ascorbic acid and alpha-tocopherol supplementations on serum leptin, tumor necrosis factor alpha, and serum amyloid A levels in individuals with type 2 diabetes mellitus.
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OBJECTIVE
Diabetes mellitus Type 2 is one of the most widespread chronic metabolic diseases. In most cases, this type of diabetes is associated with alterations in levels of some inflammatory cytokines and hormones. Considering anti-inflammatory properties of plant extracts rich in ascorbic acid
Protection against adriamycin-induced skin necrosis in the rat by dimethyl sulfoxide and alpha-tocopherol.
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Extravasation of Adriamycin during i.v. infusion can cause serious local complications. We have used a rat skin model to study the protection afforded by dimethyl sulfoxide and alpha-tocopherol (vitamin E) against Adriamycin-induced skin necrosis. Topical daily application of 1 ml dimethyl sulfoxide
Alpha-tocopherol induces expression of connective tissue growth factor and antagonizes tumor necrosis factor-alpha-mediated downregulation in human smooth muscle cells.
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The effect of alpha-tocopherol treatment on gene expression in human aortic vascular smooth muscle cells was analyzed by gene expression arrays. The expression of the connective tissue growth factor (CTGF) gene was induced by alpha-tocopherol 1.8-fold in gene array experiments, and similar results
Potential Protective Effect of Dietary Intake of Non- α-Tocopherols on Cellular Aging Markers Mediated by Tumor Necrosis Factor- α in Prediabetes: A Cross-Sectional Study of Chinese Adults
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It remains unknown how different glucose tolerance status affects the relationships between dietary intake of different tocopherol isoforms (α-, β-, γ-, and δ-tocopherol) and cellular aging, oxidative stress, and inflammatory markers. The authors conducted a
Protection by alpha-tocopherol against skin necrosis induced by doxorubicin hydrochloride.
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Extravasation of doxorubicin hydrochloride during i.v. infusions can cause serious local complications due to the action of free radicals which are produced as a result of this leakage. An experiment was carried out using female Wistar rats to study the protective effect of alpha-tocopherol against
Inhibitory effects of tocopherols on expression of the cyclooxygenase-2 gene in RAW264.7 cells stimulated by lipopolysaccharide, tumor necrosis factor-α or Porphyromonas gingivalis fimbriae.
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BACKGROUND
Tocopherols, which include α-, β-, γ-, and δ-tocopherol, protect cells against harmful free radicals and play an important role in preventing many human diseases such as cancer, inflammatory disorders, and ageing itself. However, the causal relationships between periodontal or oral
Alpha-tocopherol decreases tumor necrosis factor-alpha mRNA and protein from activated human monocytes by inhibition of 5-lipoxygenase.
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Cardiovascular disease is the leading cause of morbidity in Westernized populations. Low levels of alpha-tocopherol (AT) are associated with increased incidence of atherosclerosis and increased intakes appear to be protective. AT supplementation decreases interleukin 1 and 6 release from human
Changes of lipid peroxides and alpha-tocopherol in rats with experimentally induced myocardial necrosis.
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Myocardial necrosis was produced in rats by injection of isoproterenol (80 mg per kg body weight). Lipid peroxides were measured by the thiobarbituric acid reaction. alpha-Tocopherol was assayed by fluorometric analysis. Immediately after isoproterenol injections, serum lipid peroxides increased and
α-Tocopherol, but Not γ-Tocopherol, Attenuates the Expression of Selective Tumor Necrosis Factor-Alpha-Induced Genes in Primary Human Aortic Cell Lines.
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Of the antioxidant vitamin E isoforms, α-tocopherol (αT) and γ-tocopherol (γT) are the most abundant in the human diet, and αT is consumed from both natural and synthetic sources. αT and γT may differentially impact inflammation and influence cardiovascular outcomes, in part by modulating gene
[Effect of preliminary administration of alpha-tocopherol and intal on the course of experimental myocardial necrosis].
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Morphofunctional state of myocardial capillary bed and serum creatine kinase were measured in 70 white rats with coronary arterial occlusion. Four-day pretreatment with alpha-tocopherol and, particularly, intal, was conductive to the improvement of micro-circulation in the ischemized myocardium via
The effect of alpha-tocopherol and Intal on heart capillary bed and lipid peroxide oxidation in experimental necrosis of the rat myocardium.
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The effect of Intal and alpha-tocopherol on the morphofunctional state of myocardial capillary bed and peroxide oxidation of lipids (POL) was studied in 160 albino rats with coronary artery occlusion. The vascular effect of Intal consisted in increasing the number of functioning capillaries and
Alpha-Tocopherol Alters Transcription Activities that Modulates Tumor Necrosis Factor Alpha (TNF-α) Induced Inflammatory Response in Bovine Cells.
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To further investigate the potential role of α-tocopherol in maintaining immuno-homeostasis in bovine cells (Madin-Darby bovine kidney epithelial cell line), we undertook in vitro experiments using recombinant TNF-α as an immuno-stimulant to simulate inflammation response in cells with or without
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