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d alpha tocopherol/некроза

Линкът е запазен в клипборда
СтатииКлинични изследванияПатенти
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Vitamin E and stress. 4. The metabolism of D-alpha-tocopherol during nutritional hepatic necrosis in the rat and the effects of selenium, methionine and unsaturated fatty acids.

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Long- and short-term D-alpha-tocopherol supplementation inhibits liver collagen alpha1(I) gene expression.

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We analyzed the role of oxidative stress on liver collagen gene expression in vivo. Long- and short-term supplementation with the lipophilic antioxidant D-alpha-tocopherol (40 IU/day for 8 wk or 450 IU for 48 h) to normal C57BL/6 mice selectively decreased liver collagen mRNA by approximately 70 and

D-α-tocopherol polyethylene glycol succinate-based redox-sensitive paclitaxel prodrug for overcoming multidrug resistance in cancer cells.

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To overcome the multidrug resistance (MDR) of P-glycoprotein (P-gp) substrate anticancer drugs, such as paclitaxel (PTX), a novel dual-functional prodrug, D-α-tocopherol polyethylene glycol succinate (TPGS) based PTX prodrug (TPGS-S-S-PTX), was synthesized here to fulfill the synergistic effect of

Administration of the tris salt of alpha-tocopheryl hemisuccinate inactivates CYP2E1, enhances microsomal alpha-tocopherol levels and protects against carbon tetrachloride-induced hepatotoxicity.

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A series of tocopherol compounds were examined for their capacity to protect against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. Of the tocopherol compounds tested in our study, only the tris salt of d-alpha-tocopheryl hemisuccinate (TS-tris) protected against CCl4-induced

Superiority of TPGS-loaded micelles in the brain delivery of vinpocetine via administration of thermosensitive intranasal gel.

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Background: Vinpocetine (VPN) is a synthetic derivative of the Vinca minor alkaloids. The drug is characterized by a short half-life, limited water solubility and high hepatic first-pass effect. The objective was to develop different lipid-based nanocarriers (NCs) loaded into a

The effects of the antioxidant α-tocopherol succinate on cisplatin-induced ototoxicity in HEI-OC1 auditory cells.

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CONCLUSIONS D-α-tocopherol succinate significantly reduced a cisplatin-induced hair cell loss in HEI-OC1 cell lines. These effects were mediated by its scavenging activity against reactive oxygen species (ROS) and inhibition of apoptosis. OBJECTIVE Alpha-tocopherol is a class of methylated phenols,

Amplification of Oxidative Stress in MCF-7 Cells by a Novel pH-Responsive Amphiphilic Micellar System Enhances Anticancer Therapy.

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The excessive increase of intracellular reactive oxygen species (ROS) makes tumor cells usually in the state of oxidative stress. Although tumor cells can adapt to this state to a certain extent by upregulating antioxidant systems, the further ROS insults disrupt the transient intracellular redox

Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of inflammatory mediators in young healthy men.

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The purpose of this study was to examine the effects of feeding docosahexaenoic acid (DHA) as triacylglycerol on the fatty acid composition, eicosanoid production, and select activities of human peripheral blood mononuclear cells (PBMNC). A 120-d study with 11 healthy men was conducted at the

NIR-to-Red Upconversion Nanoparticles with Minimized Heating Effect for Synchronous Multidrug Resistance Tumor Imaging and Therapy.

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Lanthanide-doped upconversion nanoparticles (UCNPs), especially the 808 nm activated UCNPs, are promising imaging agents for biological applications because of their minimal tissue overheating effects and low autofluorescence background. Optimizing the emission peaks located in the "biological

Muscle wasting and dedifferentiation induced by oxidative stress in a murine model of cachexia is prevented by inhibitors of nitric oxide synthesis and antioxidants.

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Muscle wasting is a critical feature of patients afflicted by AIDS or cancer. In a murine model of muscle wasting, tumor necrosis factor alpha (TNF alpha) induces oxidative stress and nitric oxide synthase (NOS) in skeletal muscle, leading to decreased myosin creatinine phosphokinase (MCK)
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