l glutathione/inflamație

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l-Glutathione enhances antioxidant capacity of hyaluronic acid and modulates expression of pro-inflammatory cytokines in human fibroblast-like synoviocytes.

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Intra-articular injection of hyaluronic acid (HA) has been widely accepted for the treatment of osteoarthritis (OA) in early stage. l-Glutathione (GSH), an antioxidant, has an anti-inflammatory effect on protecting cells from reactive oxygen species and reactive nitrogen species (ROS/RNS). In this

Selective CB2 up-regulation in women affected by endometrial inflammation.

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Endometritis is defined as an inflammation of the endometrial mucosa of the uterus. In endometritis large amounts of toxic mediators, including nitric oxide (NO) are released by inflammatory cells. As a consequence of nitric oxide-dependent injury, the cells respond by triggering protective

Relevance of Erk1/2-PI3K/Akt signaling pathway in CEES-induced oxidative stress regulates inflammation and apoptosis in keratinocytes.

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2-Chloroethyl ethyl sulfide (CEES) is a well-known chemical warfare agent that induces cellular stress in exposed individuals. However, molecular mechanisms of CEES-induced oxidative stress-mediated metabolic deregulation are not clearly elucidated. Here we investigated CEES-induced free radical

Intermittent Hypoxia Contributes to the Lung Damage by Increased Oxidative Stress, Inflammation, and Disbalance in Protease/Antiprotease System.

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Intermittent hypoxia as a surrogate of obstructive sleep apnea is associated with different cardiovascular complications. However, the effects of intermittent hypoxia on the lung tissue are less known. Therefore, the aim of our present study was to investigate if intermittent hypoxia may influence

Hypoxia-induced endothelial dysfunction in apolipoprotein E-deficient mice; effects of infliximab and L-glutathione.

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OBJECTIVE Obstructive sleep apnoea (OSA) has been implicated as a risk factor for atherosclerosis. The aim of our study was to examine the effects of chronic intermittent hypoxia in apoE-/- mice serving as model of OSA on endothelial dysfunction and oxidative stress and to evaluate the reversibility

Oral reduced L-glutathione improves growth in pediatric cystic fibrosis patients.

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OBJECTIVE Consensus nutritional guidelines for patients with cystic fibrosis (CF) recommend aggressive treatment of growth failure. Oral reduced glutathione (GSH) has been shown to improve cachexia and case reports have demonstrated improved growth in pediatric patients with CF. No controlled

Loss of p53 in stromal fibroblasts enhances tumor cell proliferation through nitric-oxide-mediated cyclooxygenase 2 activation.

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Overexpression of cyclooxygenase 2 (COX-2) by stromal fibroblasts plays a critical role in the early stage of carcinogenesis. COX-2 expression is thought to be positively or negatively regulated by inflammatory chemical mediators or tumor suppressors. In this study, the contributions of inducible

Divergent effects of nitric oxide on airway epithelial cell activation.

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Nitric oxide (NO*) is a gaseous mediator synthesized by nitric oxide synthases. NO* is involved in the modulation of inflammation, but its role in airway inflammation remains controversial. We investigated the role of NO* in the synthesis of the chemokines interleukin-8 and monocyte chemotactic

Flunisolide attenuates nitric oxide-induced DNA damage in rat trachea epithelial cells.

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In asthma the bronchial epithelium is highly abnormal, with various structural changes. As a consequence, the epithelium becomes an important source of inflammatory mediators that contribute to the ongoing inflammation and remodeling responses occurring in asthma. Compared with normal individuals,

High-affinity pan-specific monoclonal antibodies that target cysteinyl leukotrienes and show efficacy in an acute model of colitis.

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Cysteinyl leukotrienes (CysLTs) are a small family of biological signaling lipids produced by active leukocytes that contribute to diverse inflammatory disease states as a consequence of their engagement with dedicated G protein-coupled receptors. Immunization of mice with a CysLT-modified hapten

Dimethyl fumarate modulates neutrophil extracellular trap formation in a glutathione and superoxide-dependent manner.

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BACKGROUND Neutrophil (polymorphonuclear) granulocytes (PMN) have been shown to contribute to the pathogenesis of psoriasis by releasing interleukin-17 and LL37-DNA complexes via neutrophil extracellular traps (NETs), webs of chromatin strands decorated with antimicrobial peptides, in psoriatic

The nonenzymatic reactivity of the acyl-linked metabolites of mefenamic acid toward amino and thiol functional group bionucleophiles.

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Mefenamic acid (MFA), a carboxylic acid-containing nonsteroidal anti-inflammatory drug, is metabolized into the chemically-reactive MFA-1-O-acyl-glucuronide (MFA-1-O-G), MFA-acyl-adenylate (MFA-AMP), and the MFA-S-acyl-coenzyme A (MFA-CoA), all of which are electrophilic and capable of acylating

Free-radical degradation of high-molar-mass hyaluronan induced by ascorbate plus cupric ions: evaluation of antioxidative effect of cysteine-derived compounds.

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Based on our previous findings, the present study has focused on free-radical-mediated degradation of the synovial biopolymer hyaluronan. The degradation was induced in vitro by the Weissberger's system comprising ascorbate plus cupric ions in the presence of oxygen, representing a model of the

Nitric oxide modulates expression of extracellular matrix genes linked to fibrosis in kidney mesangial cells.

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Mesangial cells are thought to be important mediators of glomerular inflammation and fibrosis. Studies have established a direct role for nitric oxide (NO) in the regulation of gene expression in mesangial cells. Representational difference analysis was used to investigate changes in gene expression

IκB kinase-driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease.

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BACKGROUND Nuclear factor-κB (NF-κB) is a transcriptional factor of different inflammatory patterns involved in asthma and chronic obstructive pulmonary disease (COPD) that is tightly controlled by IκB kinase (IKK) complex. OBJECTIVE We investigated the dysregulation of IKK-driven NF-κB activation

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