tocopherol/воспаление

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N-acetylcysteine and alpha-tocopherol reverse the inflammatory response in activated rat Kupffer cells.

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Activation of the resident macrophage populations of the reticuloendothelial system is a key component of the complex pathophysiology of sepsis. Macrophage activation leads to production and secretion of inflammatory mediators such as cytokines, vasoactive substances, free radicals, and chemokines,

Oxidative stress, inflammation, and diabetic vasculopathies: the role of alpha tocopherol therapy.

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The diabetic state confers an increased propensity to accelerated atherogenesis. In addition to the established risk factors, there is evidence for increased oxidative stress and inflammation in diabetes. Increased oxidative stress is manifested by increased lipid peroxidation (e.g. increased

Variants in the genes encoding TNF-α, IL-10, and GSTP1 influence the effect of α-tocopherol on inflammatory cell responses in healthy men.

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BACKGROUND Despite evidence of antioxidant effects of vitamin E in vitro and in animal studies, large, randomized clinical trials have not substantiated a benefit of vitamin E in reducing inflammation in humans. An individual's genetic background may affect the response to α-tocopherol

Effects of combination tocopherols and alpha lipoic acid therapy on oxidative stress and inflammatory biomarkers in chronic kidney disease.

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OBJECTIVE Although increased oxidative stress and inflammation are highly prevalent in chronic kidney disease (CKD), few studies have investigated whether oral antioxidant therapy can alter markers of inflammation or oxidative stress in patients with CKD. The purpose of this study was to investigate

Comment on "Differential Effects of MitoVitE, α-Tocopherol and Trolox on Oxidative Stress, Mitochondrial Function and Inflammatory Signalling Pathways in Endothelial Cells Cultured under Conditions Mimicking Sepsis , Antioxidants 2020, 9(3), 195"

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Minter, B.E. et al. recently published an article titled "Differential Effects of MitoVitE, α-Tocopherol and Trolox on Oxidative Stress, Mitochondrial Function and Inflammatory Signalling Pathways in Endothelial Cells Cultured under Conditions Mimicking Sepsis" [1][...].

Analysis of plasma tocopherols alpha, gamma, and 5-nitro-gamma in rats with inflammation by HPLC coulometric detection.

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Reactive nitrogen oxide species (RNOS) have been implicated as effector molecules in inflammatory diseases. There is emerging evidence that gamma-tocopherol (gammaT), the major form of vitamin E in the North American diet, may play an important role in these diseases. GammaT scavenges RNOS such as

Alpha-, gamma- and delta-tocopherols reduce inflammatory angiogenesis in human microvascular endothelial cells.

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Vitamin E, a micronutrient (comprising alpha-, beta-, gamma- and delta-tocopherols, alpha-, beta-, gamma- and delta-tocotrienols), has documented antioxidant and non-antioxidant effects, some of which inhibit inflammation and angiogenesis. We compared the abilities of alpha-, gamma- and

Tocopherol supplementation reduces NO production and pulmonary inflammatory response to bleomycin.

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Bleomycin causes acute lung injury through production of reactive species and initiation of inflammation. Previous work has shown alteration to the production of reactive oxygen species results in attenuation of injury. Vitamin E, in particular, γ-tocopherol, isoform, has the potential to scavenge

α-Tocopherol protected against cobalt nanoparticles and cocl2 induced cytotoxicity and inflammation in Balb/3T3 cells.

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BACKGROUND Currently, tissue damage induced by cobalt nanoparticles (CoNPs) and cobalt ions (Co2+) are the most serious adverse effect in the patients with metal-on-metal hip prostheses. Therefore, an urgent need exists for the identification of the mechanisms and the development of therapeutic

Alpha-tocopherol attenuates NFkappaB activation and pro-inflammatory cytokine production in brain and improves recovery from lipopolysaccharide-induced sickness behavior.

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This study was conducted to determine if alpha-tocopherol facilitates recovery from lipopolysaccharide (LPS)-induced sickness behavior through a NFkappaB-dependent mechanism. In the first study, 3 daily intraperitoneal (i.p.) injections of alpha-tocopherol (20 mg) improved recovery from sickness

[Markers of lipid peroxidation, inflammatory proteins and plasma tocopherols in homozygotic and heterozygotic sickle cell anemia].

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Lipoperoxidation final products represented by the TBARS (substances reacting with the Thiobarbituric acid), inflammatory reaction proteins and sera tocopherol have been studied in homozygous forms as well as in heterozygous forms of sickle cell diseases. The significant increase of TBARS (P <

Patterns of dietary intake and serum carotenoid and tocopherol status are associated with biomarkers of chronic low-grade systemic inflammation and cardiovascular risk.

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Dietary modification may affect inflammatory processes and protect against chronic disease. In the present study, we examined the relationship between dietary patterns, circulating carotenoid and tocopherol concentrations, and biomarkers of chronic low-grade systemic inflammation in a 10-year

Dietary RRR-α-tocopherol succinate attenuates lipopolysaccharide-induced inflammatory cytokines secretion in broiler chicks.

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The anti-inflammatory effects of two esters of a-tocopherol (α-TOH), all-rac-α-TOH acetate (DL-α-TOA) and RRR-α-TOH succinate (D-α-TOS), on broilers repeatedly challenged with lipopolysaccharide (LPS) were investigated. Three hundred and twenty 1-d-old broiler chicks were allotted into four

A new wrinkle on topical vitamin E and photo-inflammation: Mechanistic studies of a hydrophilic gamma-tocopherol derivative compared with alpha-tocopherol.

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The antioxidant function of vitamin E is thought to mediate its photo-protective effects. Cyclooxygenase-2 (COX-2) is an important mediator of early photo-inflammation. Thus, the ability of gamma-tocopherol to inhibit COX-2 activity independently of its antioxidant function raises important

Aerosol-administered alpha-tocopherol attenuates lung inflammation in rats given lipopolysaccharide intratracheally.

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Intrapulmonary administration of bacterial lipopolysaccharide (LPS) induces a well-characterized lung inflammatory response involving alveolar macrophage activation, proinflammatory cytokine elaboration, and neutrophil influx. Vitamin E, a lipophilic antioxidant consisting of a family that includes

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