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Oldal 1 tól től 1318 eredmények
Biaryl amide compounds reduce the inflammatory response in macrophages by regulating Dectin-1.
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Macrophages are archetypal innate immune cells that play crucial roles in the recognition and phagocytosis of invading pathogens, which they identify using pattern recognition receptors (PRRs). Dectin-1 is essential for antifungal immune responses, recognizing the fungal cellular component β-glucan,
N-(4-Tertiarybutylphenyl)-4-(3-cholorphyridin-2-yl)tetrahydropyrazine -1(2H)-carbox-amide (BCTC), a novel, orally effective vanilloid receptor 1 antagonist with analgesic properties: II. in vivo characterization in rat models of inflammatory and neuropathic pain.
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The vanilloid receptor 1 (VR1) is a cation channel expressed predominantly by nociceptive sensory neurons and is activated by a wide array of pain-producing stimuli, including capsaicin, noxious heat, and low pH. Although the behavioral effects of injected capsaicin and the VR1 antagonist
Identification and Quantification of Potential Anti-inflammatory Hydroxycinnamic Acid Amides from Wolfberry.
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Wolfberry or Goji berry, the fruit of Lycium barbarum, exhibits health-promoting properties that leads to an extensive study of their active components. We synthesized a set of hydroxycinnamic acid amide (HCCA) compounds, including trans-caffeic acid, trans-ferulic acid, and
Inhibition of Myeloperoxidase by N-Acetyl Lysyltyrosylcysteine Amide Reduces Oxidative Stress-Mediated Inflammation, Neuronal Damage, and Neural Stem Cell Injury in a Murine Model of Stroke.
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Recent studies suggest that myeloperoxidase (MPO)-dependent oxidative stress plays a significant role in brain injury in stroke patients. We previously showed that N-acetyl lysyltyrosylcysteine amide (KYC), a novel MPO inhibitor, significantly decreased infarct size, blood-brain barrier leakage,
Inhibition of fatty acid amide hydrolase suppresses referred hyperalgesia induced by bladder inflammation.
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OBJECTIVE
• To determine (i) the presence of fatty acid amide hydrolase (FAAH) in the urinary bladder; (ii) whether or not endogenous fatty acid ethanolamides are synthesized by the bladder; (iii) the effects of FAAH inhibition on referred hyperalgesia associated with acute bladder inflammation in
Inhibition of fatty acid amide hydrolase produces PPAR-alpha-mediated analgesia in a rat model of inflammatory pain.
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OBJECTIVE
We have previously demonstrated antinociceptive effects of fatty acid amide hydrolase (FAAH) inhibition that were accompanied by increases in the levels of endocannabinoids (ECs) in the hind paw. Here, the effects of the FAAH inhibitor URB597
Inhibitors of fatty acid amide hydrolase reduce carrageenan-induced hind paw inflammation in pentobarbital-treated mice: comparison with indomethacin and possible involvement of cannabinoid receptors.
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The in vivo effect of inhibitors of fatty acid amide hydrolase (FAAH) upon oedema volume and FAAH activity was evaluated in the carrageenan induced hind paw inflammation model in the mouse. Oedema was measured at two time points, 2 and 4 h, after intraplantar injection of carrageenan to
Aromatic amide derivatives of 5,6-dimethoxy-2,3-dihydro-1H-inden(-1-yl)acetic acid as anti-inflammatory agents free of ulcerogenic liability.
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Amide derivatives of 5,6-dimethoxy-2,3-dihydro-1H-inden(-1-yl)acetic acid were synthesized and evaluated for their anti-inflammatory and analgesic activity. Few selected compounds were also screened for their antipyretic, anti-arthritic, and ulcerogenic potential. Most of the compounds exhibited
sec-Butylpropylacetamide (SPD), a new amide derivative of valproic acid for the treatment of neuropathic and inflammatory pain.
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Chronic pain is a multifactorial disease comprised of both inflammatory and neuropathic components that affect ∼20% of the world's population. sec-Butylpropylacetamide (SPD) is a novel amide analogue of valproic acid (VPA) previously shown to possess a broad spectrum of anticonvulsant activity. In
Synthesis and biological evaluation of amide derivatives of (5,6-dimethoxy-2,3-dihydro-1H-inden-1-yl)acetic acid as anti-inflammatory agents with reduced gastrointestinal ulcerogenecity.
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A variety of amide derivatives of (5,6-dimethoxy-2,3-dihydro-1H-inden-1-yl)acetic acid were synthesized and screened for their analgesic and anti-inflammatory activities. The compounds were found to have longer activity profile exceeding that of indomethacin in carrageenan-induced rat paw edema
Synthesis and study of anti-inflammatory activity of some novel cyclophane amides.
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Macrocyclic di- and tetra-amides with thia- and oxylinkages were synthesized and screened for in vitro anti-inflammatory activity. Cyclophane diamide 15 showed a dose-dependent activity, while the other cyclophane amides 16-20 exhibited mild activity.
Ester and amide prodrugs of ibuprofen and naproxen: synthesis, anti-inflammatory activity, and gastrointestinal toxicity.
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Ester and amide prodrugs of ibuprofen (1) and naproxen (16) were synthesized and evaluated for anti-inflammatory activity and gastrointestinal toxicity. The chemical structure of the prodrugs was varied in terms of lipophilicity and reactivity toward hydrolysis. Inhibition of acetic acid-induced
Synthesis and anti-inflammatory activity of 5-(1,4-dihydropyridyl)-tetrazol-2-acetic acids, esters and amides.
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Thirteen 5-[3-(1,4-dihydropyridyl)]-2H-tetrazol-2-acetic acids (18-30), seventeen esters (4-17, 32, 35, 41) and eight amides (31, 32-34, 36-40) were synthesized in order to investigate the effect of alpha-substituents (R1 = H, Me) and 1,4-dihydropyridyl substituents (R2 = aryl, alkyl; R3 = phenoxy,
Synthesis of N-[4-(propyl)cyclohexyl]-amides with anti-inflammatory and analgesic activities.
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Seventeen (un)substituted N-[4-(propyl)cyclohexyl]-amides (6a-h, 7a-h and 8) were synthesized and tested as anti-inflammatory and analgesic agents. The substituents on the aromatic ring were chosen in order to study the influence of electron-withdrawing or electron-donating residues, that change the
Characterization of the in vitro anti-inflammatory activity of AL-5898 and related benzopyranyl esters and amides.
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Selected ester- (AL-5898 and AL-8417) and amide-linked benzopyran analogues (AL-7538 and AL-12615) were evaluated in vitro for their ability to inhibit key enzymes/processes of the inflammatory response. AL-7538 and AL-12615 exhibited weak intrinsic cyclooxygenase inhibitory activity (IC50 = 13
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