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trans 2 nonenal/inflamación
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Página 1 desde 19 resultados
4-Hydroxy-Trans-2-Nonenal in the Regulation of Anti-Oxidative and Pro-Inflammatory Signaling Pathways.
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Recent studies indicate that 4-hydroxy-trans-2-nonenal (HNE), a major oxidative stress triggered lipid peroxidation-derived aldehyde, plays a critical role in the pathophysiology of various human pathologies including metabolic syndrome, diabetes, cardiovascular, neurological, immunological, and
Lipid mediator interplay: resolvin D1 attenuates inflammation evoked by glutathione-conjugated lipid peroxidation products.
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Non-enzymatic oxidation of cellular lipids, one of the characteristic features of inflammation, leads to formation of highly reactive and toxic alpha,beta-unsaturated aldehydes, such as 4-hydroxy-trans-2-nonenal (HNE). Conjugation of HNE with reduced glutathione (GS-HNE) is widely believed to
Resolvin D1 controls inflammation initiated by glutathione-lipid conjugates formed during oxidative stress.
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OBJECTIVE
Inflammation is associated with oxidative stress and local generation of lipid peroxidation-derived aldehydes, such as 4-hydroxy-trans-2-nonenal (HNE). In most tissues, HNE is readily conjugated with glutathione and presently it is unknown whether glutathionyl-HNE (GS-HNE) plays a
Lipid peroxidation product 4-hydroxy-trans-2-nonenal causes endothelial activation by inducing endoplasmic reticulum stress.
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Lipid peroxidation products, such as 4-hydroxy-trans-2-nonenal (HNE), cause endothelial activation, and they increase the adhesion of the endothelium to circulating leukocytes. Nevertheless, the mechanisms underlying these effects remain unclear. We observed that in HNE-treated human umbilical vein
Aldose reductase mediates the lipopolysaccharide-induced release of inflammatory mediators in RAW264.7 murine macrophages.
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Abnormal production of inflammatory cytokines and chemokines is a key feature of bacterial endotoxin, lipopolysaccharide (LPS)-induced inflammation, and cytotoxicity; however, the mechanisms regulating production of inflammatory markers remain unclear. Herein, we show that inhibition of the
Regulation of NF-κB-induced inflammatory signaling by lipid peroxidation-derived aldehydes.
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Oxidative stress plays a critical role in the pathophysiology of a wide range of diseases including cancer. This view has broadened significantly with the recent discoveries that reactive oxygen species initiated lipid peroxidation leads to the formation of potentially toxic lipid aldehyde species
Aldose reductase inhibition suppresses oxidative stress-induced inflammatory disorders.
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Oxidative stress-induced inflammation is a major contributor to several disease conditions including sepsis, carcinogenesis and metastasis, diabetic complications, allergic asthma, uveitis and after cataract surgery posterior capsular opacification. Since reactive oxygen species (ROS)-mediated
Identification of biochemical pathways for the metabolism of oxidized low-density lipoprotein derived aldehyde-4-hydroxy trans-2-nonenal in vascular smooth muscle cells.
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Oxidation of low-density lipoproteins (LDL) generates high concentrations of unsaturated aldehydes, such as 4-hydroxy trans-2-nonenal (HNE). These aldehydes are mitogenic to vascular smooth muscle cells and sustain a vascular inflammation. Nevertheless, the processes that mediate and regulate the
Involvement of aldose reductase in the metabolism of atherogenic aldehydes.
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Phospholipid peroxidation generates a variety of aldehydes, which includes free saturated and unsaturated aldehydes, and aldehydes that remain esterified to the phosphoglyceride backbone - the so-called 'core' aldehydes. However, little is known in regarding the vascular metabolism of these
Acrolein induces vasodilatation of rodent mesenteric bed via an EDHF-dependent mechanism.
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Acrolein is generated endogenously during lipid peroxidation and inflammation and is an environmental pollutant. Protein adducts of acrolein are detected in atherosclerotic plaques and neurons of patients with Alzheimer's disease. To understand vascular effects of acrolein exposure, we studied
Chronic oral exposure to the aldehyde pollutant acrolein induces dilated cardiomyopathy.
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Environmental triggers of dilated cardiomyopathy are poorly understood. Acute exposure to acrolein, a ubiquitous aldehyde pollutant, impairs cardiac function and cardioprotective responses in mice. Here, we tested the hypothesis that chronic oral exposure to acrolein induces inflammation and
Possible role of aldehydic lipid peroxidation products as chemoattractants.
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Previous studies showed that the lipid peroxidation product 4-hydroxy-trans-2-nonenal (HNE) stimulates the rat neutrophil oriented migration in vitro within a micromolar range. Its effect is weak with respect to other known chemoattractants, but highly significant on the basis of a two-way analysis
CD36 deletion improves recovery from spinal cord injury.
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CD36 is a pleiotropic receptor involved in several pathophysiological conditions, including cerebral ischemia, neurovascular dysfunction and atherosclerosis, and recent reports implicate its involvement in the endoplasmic reticulum stress response (ERSR). We hypothesized that CD36 signaling
Toxic oxygenated alpha,beta-unsaturated aldehydes and their study in foods: a review.
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The oxidation of lipids containing polyunsaturated omega-3 or omega-6 acyl groups, such as docosahexenoic, eicosapentenoic, linolenic, arachidonic, or linoleic groups, and of the corresponding fatty acids, generates among other compounds alpha,beta -unsaturated aldehydes supporting different
Metals, oxidative stress and neurodegenerative disorders.
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The neurodegenerative diseases, Alzheimer's disease (AD) and Parkinson's disease (PD), are age-related disorders characterized by the deposition of abnormal forms of specific proteins in the brain. AD is characterized by the presence of extracellular amyloid plaques and intraneuronal neurofibrillary
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