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anti inflammatory/hypoxia
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Statin-induced expression of CD59 on vascular endothelium in hypoxia: a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis.
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Hypoxia, which leads to dysfunctional cell metabolism, and complement activation both play central roles in the pathogenesis of rheumatoid arthritis (RA). Recent studies have reported that mice deficient for the complement-inhibitory protein CD59 show enhanced susceptibility to antigen-induced
Chronic Oxytocin treatment has long lasting therapeutic potential in a rat model of neonatal hypercapnic-hypoxia injury, through enhanced GABAergic signaling and by reducing hippocampal gliosis with its anti-inflammatory feature
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Previous studies have shown that, oxytocin has anticonvulsant and neuroprotective effects. One of the most important complications of Hypercapnic-hypoxia is drug resistance epilepsy. Effects of chronic intraperitoneal oxytocin treatment on gliosis, neuroinflammation and seizure activity was
[Change in the anti-inflammatory activity of nonsteroidal antiphlogistics in conditions of acute hypoxic hypoxia].
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It has been shown on animals with experimental histamine edema under acute hypoxic hypoxia that anti-inflammatory properties of the known non-steroidal antiphlogistics and new derivatives of fumaric acid heterylamides administered in a dose of 10% of the LD50 underwent changes. At "altitudes" of
Anti-inflammatory agent, dexamethasone, does not affect exercise-induced arterial hypoxemia in Thoroughbreds.
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In view of the suggestion that pulmonary injury-induced release of histamine and/or other chemical mediators from airway inflammatory and mast cells contribute to the exercise-induced arterial hypoxemia (EIAH) in human athletes, we examined the effects of pretreatment with a potent anti-inflammatory
Hypoxia reduces the expression and anti-inflammatory effects of peroxisome proliferator-activated receptor-gamma in human proximal renal tubular cells.
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BACKGROUND
Peroxisome proliferator-activated receptor (PPAR)-gamma may counteract tissue fibrosis via its anti-inflammatory actions, while hypoxia, a new pro-fibrotic factor, reportedly modifies PPAR-gamma expression. However, the effects of hypoxia on the expression and anti-inflammatory actions of
Naproxen, a Nonsteroidal Anti-Inflammatory Drug, Can Affect Daily Hypobaric Hypoxia-Induced Alterations of Monoamine Levels in Different Areas of the Brain in Male Rats.
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Goswami, Ananda Raj, Goutam Dutta, and Tusharkanti Ghosh. Naproxen, a nonsteroidal anti-inflammatory drug can affect daily hypobaric hypoxia-induced alterations of monoamine levels in different areas of the brain in male rats. High Alt Med Biol. 17:133-140, 2016.-The oxidative stress (OS)-induced
Anti-inflammatory effect of erythropoietin pretreatment on cardiomyocytes with hypoxia/reoxygenation injury and the possible mechanism.
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OBJECTIVE
To investigate the anti-inflammatory effect of erythropoietin (EPO) pretreatment on cardiomyocytes exposed to hypoxia/reoxygenation injury (H/R) and explore the possible mechanism.
METHODS
The cultured neonatal rats?ventricular cardiomyocytes were divided randomly into 4 groups, control
The specific expression of hypoxia inducible factor-1alpha in human gastric mucosa induced by nonsteroidal anti-inflammatory drugs.
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BACKGROUND
Hypoxia is a cause of gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs (NSAIDs). The expression of hypoxia inducible factor-1alpha (HIF-1alpha) reflects the status of tissue ischaemia.
OBJECTIVE
To investigate the effect of NSAID administration on the expression of
The δ-Opioid Receptor Differentially Regulates MAPKs and Anti-inflammatory Cytokines in Rat Kidney Epithelial Cells Under Hypoxia.
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Hypoxic injury is one of the most important factors in progressive kidney disorders. Since we have found that δ-opioid receptor (DOR) is neuroprotective against hypoxic stress through a differential regulation of mitogen-activated protein kinases (MAPKs) and anti-inflammatory cytokines, we asked if
[Effects of hypoxia on the expression of glucocorticoid receptor and the anti-inflammatory action of dexamethasone in human alveolar epithelial cells].
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OBJECTIVE
To study the changes in the expression levels of two isoforms of glucocorticoid receptor (GRα and GRβ) and the anti-inflammatory effect of dexamethasone in human alveolar epithelial cell under hypoxic conditions.
METHODS
Human alveolar epithelial cell line A549 was used as the model. Cells
Pharmacologic stimulation of the nicotinic anti-inflammatory pathway modulates gut and lung injury after hypoxia-reoxygenation injury.
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OBJECTIVE
Pre-injury vagal nerve stimulation protects against gut and lung injury after experimental hemorrhagic shock (HS). This likely occurs via the cholinergic anti-inflammatory pathway and the α7 nicotinic acetylcholine receptor (α7nAChR). We hypothesized that, in an in vitro model, either
The Delta Opioid Peptide DADLE Represses Hypoxia-Reperfusion Mimicked Stress Mediated Apoptotic Cell Death in Human Mesenchymal Stem Cells in Part by Downregulating the Unfolded Protein Response and ROS along with Enhanced Anti-Inflammatory Effect.
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Hypoxia-reperfusion (H/R) emblems a plethora of pathological conditions which is potent in contributing to the adversities encountered by human mesenchymal stem cells (hMSCs) in post-transplant microenvironment, resulting in transplant failure. D-Alanine 2, Leucine 5 Enkephaline (DADLE)-mediated
Mechanisms of vascular endothelial cell injury in response to intermittent and/or continuous hypoxia exposure and protective effects of anti-inflammatory and anti-oxidant agents.
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The connectivity map links iron regulatory protein-1-mediated inhibition of hypoxia-inducible factor-2a translation to the anti-inflammatory 15-deoxy-delta12,14-prostaglandin J2.
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Hypoxia-inducible factors 1 and 2 (HIF1 and HIF2) are heterodimeric transcription factors consisting of alpha regulatory subunits and a constitutively expressed beta subunit. The expression of alpha regulatory subunits is promoted by hypoxia, cancer-associated mutations, and inflammatory cytokines.
The anti-inflammatory effect of baicalin on hypoxia/reoxygenation and TNF-alpha induced injury in cultural rat cardiomyocytes.
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The aim of present study was to investigate the effect of baicalin on hypoxia/reoxygenation (H/R) injury in cardiomyocytes and the mechanisms involved, particularly in relation to cytokines. The cardiomyocytes for the H/R groups were placed into a hypoxic chamber for 12 h and then underwent
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