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dodecanoic acid/infiammazione
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 39 risultati
Dillenia suffruticosa L. Impedes Carbon Tetrachloride-Induced Hepatic Damage by Modulating Oxidative Stress and Inflammatory Markers in Rats.
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Dillenia suffruticosa L. (Dilleniaceae) is used in traditional medicine for protection against various diseases. The current study was designed to investigate the bioactive compounds and hepatoprotective potential of methanol leaves extract of D. suffruticosa against carbon tetrachloride
A Novel Antidiabetic Monomers Combination Alleviates Insulin Resistance Through Bacteria-Cometabolism-Inflammation Responses.
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The present study sought to examine the therapeutic effect of a novel antidiabetic monomer combination (AMC) in treating type 2 diabetes mellitus (T2DM); while also elucidating the potential functional mechanism. Male C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to establish T2DM. The
Soluble epoxide hydrolase activity regulates inflammatory responses and seizure generation in two mouse models of temporal lobe epilepsy.
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Neuroinflammation is known to be involved in epileptogenesis with unclear mechanisms. Inhibition of soluble epoxide hydrolase (sEH) seems to offer anti-inflammatory protection to ischemic brain injury in rodents. Thus, it is hypothesized that sEH inhibition might also affect the neuroinflammatory
Attenuation of tobacco smoke-induced lung inflammation by treatment with a soluble epoxide hydrolase inhibitor.
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Changes in the lungs due to smoking include inflammation, epithelial damage, and remodeling of the airways. Airway inflammation is likely to play a critical role in the genesis and progression of tobacco smoke-induced airway disease. Soluble epoxide hydrolase (sEH) is involved in the metabolism of
Soluble epoxide hydrolase inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid, represses human aortic smooth muscle cell proliferation and migration by regulating cell death pathways via the mTOR signaling.
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The soluble epoxide hydrolase (sEH) is a molecule necessary for the metabolism of endogenous constituents implicated in blood pressure regulation and vascular inflammation. Scientific evidences indicate that sEH inhibitors such as 12-(3-Adamantan-1-yl-ureido)-dodecanoic acid (AUDA) could be a
Design of bioavailable derivatives of 12-(3-adamantan-1-yl-ureido)dodecanoic acid, a potent inhibitor of the soluble epoxide hydrolase.
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The soluble epoxide hydrolase (sEH) plays an important role in the metabolism of endogenous chemical mediators involved in blood pressure regulation and vascular inflammation. 12-(3-Adamantan-1-yl-ureido)-dodecanoic acid (AUDA, 1) is a very active inhibitor of sEH both in vitro and in vivo. However,
Inhibition of soluble epoxide hydrolase does not protect against endotoxin-mediated hepatic inflammation.
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Epoxyeicosatrienoic acids (EETs) are derived from cytochrome P450-catalyzed epoxygenation of arachidonic acid and have emerged as important mediators of numerous biological effects. The major elimination pathway for EETs is through soluble epoxide hydrolase (sEH)-catalyzed metabolism to
Colletopeptides A-D, Anti-inflammatory Cyclic Tridepsipeptides from the Plant Endophytic Fungus Colletotrichum sp. S8.
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Four new hybrid peptide-polyketide cyclic tridepsipeptides, colletopeptides A-D (1-4), were isolated and characterized from the endophytic fungus Colletotrichum sp. S8 derived from the stems of Rubia podantha with the guidance of LC-UV-MS detection. Their structures were elucidated by extensive
Soluble epoxide hydrolase inhibition enhances anti-inflammatory and antioxidative processes, modulates microglia polarization, and promotes recovery after ischemic stroke.
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Vascular repair and anti-inflammatory effects of soluble epoxide hydrolase inhibitor.
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Kawasaki disease (KD) is the leading cause of acquired heart disease in pediatric patients in developed countries. Coronary artery aneurysms and myocardial infarction may occur if the disease remains untreated. An estimated 10-20% of KD patients do not respond to intravenous gamma globulin (IVIG),
17,18-epoxyeicosatetraenoic acid targets PPARγ and p38 mitogen-activated protein kinase to mediate its anti-inflammatory effects in the lung: role of soluble epoxide hydrolase.
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This study sought to assess putative pathways involved in the anti-inflammatory effects of 17,18-epoxyeicosatetraenoic acid (17,18-EpETE), as measured by a decrease in the contractile reactivity and Ca(2+) sensitivity of TNF-α-pretreated human bronchi. Tension measurements performed in the presence
Pharmacokinetic optimization of four soluble epoxide hydrolase inhibitors for use in a murine model of inflammation.
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OBJECTIVE
Early soluble epoxide hydrolase inhibitors (sEHIs) such as 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA) are effective anti-hypertensive and anti-inflammatory agents in various animal models. However, their poor metabolic stability and limited water solubility make them difficult to
Enhancement of antinociception by coadministration of nonsteroidal anti-inflammatory drugs and soluble epoxide hydrolase inhibitors.
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Combination therapies have long been used to treat inflammation while reducing side effects. The present study was designed to evaluate the therapeutic potential of combination treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and previously undescribed soluble epoxide hydrolase
Epoxygenated Fatty Acids Inhibit Retinal Vascular Inflammation.
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The objective of the present study was to assess the effect of elevating epoxygenated fatty acids on retinal vascular inflammation. To stimulate inflammation we utilized TNFα, a potent pro-inflammatory mediator that is elevated in the serum and vitreous of diabetic patients. In TNFα-stimulated
Effect of PPARalpha activation of macrophages on the secretion of inflammatory cytokines in cultured adipocytes.
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The relationship between adipocytes and infiltrated macrophages in fat tissue is important for the pathogenesis of insulin resistance through the activation of cytokines. Peroxisome proliferator-activated receptors (PPARs) play a role in the regulation of cytokine secretion in these cells. We
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