There were no intraoperative or postoperative complications, nor were there any serious side effects attributable to any of the intravesically instilled agents. There was a statistically significant decrease in stent-related discomfort at the 1-hour time point in the group of patients who received intravesical ketorolac compared with the control group.
The scuticociliatosis produced by the endoparasite Philasterides dicentarchi is a severe parasitic infection of farmed turbot (Scophthalmus maximus) characterized by several histopathological effects including extensive inflammation. Indomethacin is a nonsteroidal anti-inflammatory drug that specifically inhibits synthesis of the proinflammatory mediator prostaglandins. The effect of indomethacin on the in vitro growth of P. dicentrarchi was investigated. In vitro growth of the scuticociliate was significantly inhibited by treatment with 100 microM indomethacin for 48 h. Higher concentrations of indomethacin (mM levels) did not affect the gelatinolytic activity of the cysteine proteinases of P. dicentrarchi. In vitro treatment with 25, 50 or 100 microM indomethacin for 3 days did not significantly affect the enzymatic activity of cysteine proteinases, as assayed with p-nitroanilide as substrate. Immunoblot analysis with anti-cysteine proteinase antibodies revealed an increase in proteinase expression (molecular weights of 80, 32 and 40-45 kDa) in parasite lysates originating from in vitro cultures incubated with 25 microM indomethacin for 72 h. Degradation of genomic DNA of the ciliates was observed in cultures incubated with 100 microM indomethacin for 1, 3 and 7 days. The results suggest that indomethacin is capable of inhibiting in vitro growth of the scuticociliate P. dicentrarchi by a mechanism related to the induction of programmed cell death, without affecting the enzymatic activation of parasite proteinases, which demonstrates the potential therapeutic use of this drug in the control of turbot scuticociliatosis.
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 inhibitors (sEHIs) in lipopolysaccharide (LPS)-challenged mice. NSAIDs inhibit cyclooxygenase (COX) enzymes and thereby decrease production of metabolites that lead to pain and inflammation. The sEHIs, such as 12-(3-adamantan-1-yl-ureido)-dodecanoic acid butyl ester (AUDA-BE), stabilize anti-inflammatory epoxy-eicosatrienoic acids, which indirectly reduce the expression of COX-2 protein. Here we demonstrate that the combination therapy of NSAIDs and sEHIs produces significantly beneficial effects that are additive for alleviating pain and enhanced effects in reducing COX-2 protein expression and shifting oxylipin metabolomic profiles. When administered alone, AUDA-BE decreased protein expression of COX-2 to 73 +/- 6% of control mice treated with LPS only without altering COX-1 expression and decreased PGE(2) levels to 52 +/- 8% compared with LPS-treated mice not receiving any therapeutic intervention. When AUDA-BE was used in combination with low doses of indomethacin, celecoxib, or rofecoxib, PGE(2) concentrations dropped to 51 +/- 7, 84 +/- 9, and 91 +/- 8%, respectively, versus LPS control, without disrupting prostacyclin and thromboxane levels. These data suggest that these drug combinations (NSAIDs and sEHIs) produce a valuable beneficial analgesic and anti-inflammatory effect while prospectively decreasing side effects such as cardiovascular toxicity.
The greatest reduction of hyperalgesia was observed in the group of animals treated with morphine, followed by dexamethasone, indomethacin and atenolol. Reductions in hyperalgesia were observed after drug administration ceased, except for the group of animals treated with morphine, in which there was an increase in hyperalgesia after discontinuation of the treatment.
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Salicylaldehyde 2-chlorobenzoyl hydrazone (H(2)LASSBio-466), salicylaldehyde 4-chlorobenzoyl hydrazone (H(2)LASSBio-1064) and their complexes [Zn(LASSBio-466)H(2)O](2) (1) and [Zn(HLASSBio-1064)Cl](2) (2) were evaluated in animal models of peripheral and central nociception, and acute inflammation. All studied compounds significantly inhibited acetic acid-induced writhing response. Upon coordination the anti-nociceptive activity was favored in the complex 1. H(2)LASSBio-466 inhibited only the first phase of the formalin test, while 1 was active in the second phase, like indomethacin, indicating its ability to inhibit nociception associated with the inflammatory response. Hence coordination to zinc(II) altered the pharmacological profile of H(2)LASSBio-466. H(2)LASSBio-1064 inhibited both phases but this effect was not improved by coordination. The studied compounds did not increase the latency of response in the hot plate model, indicating their lack of central anti-nociceptive activity. All compounds showed levels of inhibition of zymosan-induced peritonitis comparable or superior to indomethacin, indicating an expressive anti-inflammatory profile.
Bone metastasis is one of the major causes of cancer-related pain, and not all bone cancer pain can be effectively treated. Recently, a mouse model of bone cancer pain was introduced. To test the analgesic effects of nonsteroidal antiinflammatory drugs on bone cancer pain, the authors examined the effects of oral administration of a cyclooxygenase-1 (COX-1) selective inhibitor (SC560), a COX-2 selective inhibitor (celecoxib), and a nonselective COX inhibitor (indomethacin) on bone cancer pain and compared these effects to the effect of orally administered acetaminophen and morphine.
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It appears that STW 5, which has a pronounced efficacy in functional gastro-intestinal diseases, has no effect on septic liver and lung damage in the CLP rat model.
Preterm infants are delivered while glomerulogenesis is ongoing and may be exposed to insults, including medications that may affect renal development. Podocytes detected in the urine are an indicator of glomerular injury. The aims of this study were to determine whether preterm and term infants excrete podocytes in their urine and whether exposure to gentamicin and indomethacin increase podocyte excretion in their urine.
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The intestinal epithelium contains columnar epithelial cells (ECs) and M cells, and fucosylation of the apical surface of ECs and M cells is involved in distinguishing the two populations and in their response to commensal flora and environmental stress. Here, we show that fucosylated ECs (F-ECs) were induced in the mouse small intestine by the pro-inflammatory agents dextran sodium sulfate and indomethacin, in addition to an enteropathogen derived cholera toxin. Although F-ECs showed specificity for the M cell-markers, lectin Ulex europaeus agglutinin-1 and our monoclonal antibody NKM 16-2-4, these cells also retained EC-phenotypes including an affinity for the EC-marker lectin wheat germ agglutinin. Interestingly, fucosylation of Peyer's patch M cells and F-ECs was distinctly regulated by α(1,2)fucosyltransferase Fut1 and Fut2, respectively. These results indicate that Fut2-mediated F-ECs share M cell-related fucosylated molecules but maintain distinctive EC characteristics, Fut1 is, therefore, a reliable marker for M cells.
Rapid angiogenesis occurs as the ovulatory follicle is transformed into the corpus luteum. To determine if luteinizing hormone (LH)-stimulated prostaglandin E2 (PGE2) regulates angiogenesis in the ovulatory follicle, cynomolgus macaques received gonadotropins to stimulate multiple follicular development and chorionic gonadotropin (hCG) substituted for the LH surge to initiate ovulatory events. Before hCG, vascular endothelial cells were present in the perifollicular stroma but not amongst granulosa cells. Endothelial cells entered the granulosa cell layer 24-36 h after hCG, concomitant with the rise in follicular PGE2 and prior to ovulation, which occurs about 40 h after hCG. Intrafollicular administration of the PG synthesis inhibitor indomethacin was coupled with PGE2 replacement to demonstrate that indomethacin blocked and PGE2 restored follicular angiogenesis in a single, naturally developed monkey follicle in vivo. Intrafollicular administration of indomethacin plus an agonist selective for a single PGE2 receptor showed that PTGER1 and PTGER2 agonists most effectively stimulated angiogenesis within the granulosa cell layer. Endothelial cell tracing and three-dimensional reconstruction indicated that these capillary networks form via branching angiogenesis. To further explore how PGE2 mediates follicular angiogenesis, monkey ovarian microvascular endothelial cells (mOMECs) were isolated from ovulatory follicles. The mOMECs expressed all four PGE2 receptors in vitro. PGE2 and all PTGER agonists increased mOMEC migration. PTGER1 and PTGER2 agonists promoted sprout formation while the PTGER3 agonist inhibited sprouting in vitro. While PTGER1 and PTGER2 likely promote the formation of new capillaries, each PGE2 receptor may mediate aspects of PGE2's actions and, therefore, LH's ability to regulate angiogenesis in the primate ovulatory follicle.
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A short term, prospective cohort study.
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All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 micromol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 micromol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 micromol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro.
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Endothelium plays an important role in mediating the function of transplanted organs. The widely used University of Wisconsin solution impairs the endothelium-derived hyperpolarizing factor-mediated relaxation in coronary arteries, but little is known about effects of lung preservation on endothelium-derived hyperpolarizing factor-mediated endothelial function. This study examined the effect of organ preservation solutions on the endothelium-derived hyperpolarizing factor-mediated relaxation in the pulmonary microarteries (diameter 200 to 450 microm).
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BACKGROUND: Peroxisome proliferator-activated receptors (PPARs) are a class of nuclear transcription factors that are activated by fatty acids and their derivatives. One of these, PPARgamma, regulates responsiveness to insulin in adipose cells, and PPARgamma-activating drugs such as pioglitazone are used in the treatment of type 2 diabetes. PPARgamma acts in myeloid-lineage cells, including T-cells and macrophages, to suppress their activation and their elaboration of inflammatory molecules. PPARgamma activation also suppresses the activated phenotype in microglia, suggesting that PPARgamma-activating drugs may be of benefit in chronic neuroinflammatory diseases. Some, but not all, nonsteroidal anti-inflammatory agents (indomethacin and ibuprofen in particular) also have activating effects on PPARgamma. DISCUSSION AND CONCLUSIONS: These observations suggest on the one hand a role for PPARgamma-activating drugs in the treatment of chronic neuroinflammatory diseases-as shown for a patient with secondary progressive multiple sclerosis by Pershadsingh et al. in this issue of the Journal of Neuroinflammation-and suggest on the other hand a possible explanation for confusing and contradictory results in trials of nonsteroidal anti-inflammatory agents in Alzheimer's disease.
The ethanolic root extract of Croton zambesicus was investigated for its potential to protect gastric mucosa against ulcers induced by indomethacin, ethanol and reserpine. The anticonvulsant activity of the root extract against pentylene tetrazol (PTZ)- and picrotoxin-induced convulsion in mice was also studied. The extract (27-81 mg/kg) produced a significant (P<0.005-0.001) dose-dependent effects against the ulcerogenic effect of different agents used; indomethacin, ethanol and reserpine. The effect of the extract was lower than that of the standard drug, cimetidine (100 mg/kg) in the indomethacin and reserpine-induced ulcer models and higher than that of propranolol (40 mg/kg) in ethanol-induced ulcer model. The extract (27-81 mg/kg) could not protect mice from convulsion in both PTZ--and picrotoxin-induced convulsion. The root extract significantly (P<0.01-0.001) delayed the onset and latency of convulsion caused by PTZ and picrotoxin. The root extract possesses antiulcer and anticonvulsant properties.
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Early fluid and electrolyte imbalances may be associated with an increased risk of bronchopulmonary dysplasia.
Triphala has a promising anti-inflammatory effect in the inflamed paw of arthritis-induced rats.
The results indicate that I. sonchifolia (20 to approximately 160 g x L(-1) can contract the rat thoracic aortic rings with endothelium. The effect of contraction may enhance angiotensin converting enzyme activity and promote endothelium to synthesize angiotensin II. It has no relationship to endothelin or thromboxane A2.
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Healthy adults with body mass indices of 15-30 kg/m(2) were eligible for the study. Following intranasal ketorolac tromethamine dosing, blood samples (approximately 7 mL per sample) for pharmacokinetic assessment were obtained at 15, 30 and 45 min and 1, 1.5, 2, 4, 6, 8, 12, 15 and 24 h after dosing. Plasma ketorolac concentration versus time data were analysed to determine maximum (peak) ketorolac concentration (C(max)) and time to reach C(max) (t(max)) and estimate pharmacokinetic parameters.
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We randomly assigned 100 patients to five study groups (20 per group): control group, no injection; intra-articular (IA) ropivacaine group, IA injection of ropivacaine alone; IA MDC group, IA injection of MDC; PA MDC group, PA injection of MDC; and IA + PA MDC group, IA and PA injections of MDC. The MDC consisted of ropivacaine, morphine, ketorolac, epinephrine, and cefuroxime. The five groups were compared in terms of pain levels during the first night after surgery and on postoperative days 1, 2, and 14; patient satisfaction was assessed on postoperative day 14.
1. This study describes the effects of hypoxia on relaxing responses and cAMP production induced by the known vasodilator peptides: alphaCGRP, amylin (AMY) and adrenomedullin (AM) on isolated pig coronary arteries in vitro. 2. Hypoxic incubation increased the vasorelaxant effect of alphaCGRP (four-fold; P<0.05), AMY (3.2-fold; P<0.05), but not significantly for AM (two-fold; NS). 3. Whereas hypoxia had no effect on arterial cAMP levels, it significantly potentiated the production of cAMP stimulated of alphaCGRP and AMY, but not of AM. 4. The antagonist alphaCGRP(8-37) also exerted an increased effect in hypoxia. The Schild plot-derived pK(B) values revealed an increase in the apparent affinity of the antagonist for the CGRP(1) receptor from 7.0 to 7.2 under control conditions versus 8.0 in hypoxia. 5. Removal of endothelium, peptidase inhibitors, preincubation with the adenosine A(2A) receptor antagonist CSC (10(-3) M), the ATP-sensitive K-channel inhibitor glibenclamide (10(-5) M), the cyclooxygenase inhibitor indomethacin (10(-3) M) or NG-monomethyl-L-arginine (10(-4) M) had no effect on the alphaCGRP-induced vasorelaxation in hypoxia; neither did hypoxia influence the levels of CGRP and AM receptor mRNA. 6. We conclude that hypoxic incubation increases the relaxation and cAMP production induced by alphaCGRP and AMY in rings of porcine coronary arteries in vitro. A concomitant release of adenosine, a cyclooxygenase product, an endothelium-derived substance, activation of vascular ATP-sensitive K-channels, peptidase inhibitors or changes in CGRP and AM receptor mRNA cannot account for the changes observed in hypoxia. Moreover, alphaCGRP(8-37) showed increased affinity at the CGRP(1) receptor during hypoxia, possibly due to a conformational change at the CGRP(1) receptor site.
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Clostridium difficile-associated disease causes diarrhea to fulminant colitis and death. We investigated the role of phospholipase A2 (PLA2) inhibitors, aristolochic acid (AA), bromophenacyl bromide (BPB) and quinacrine (QUIN) on the C. difficile toxin A-induced disruption of epithelial integrity, histologic inflammatory damage and intestinal secretion. Toxin A caused severe hemorrhagic and inflammatory fluid secretion at 6-8 h in rabbit ileal segments, an effect that was significantly inhibited by QUIN (71%, P < 0.01), AA (87%, P < 0.000l) or by BPB (51%, P < 0.01). The secretory effect of toxin A was also inhibited in segments adjacent to those with AA (89%, P < 0.01). Furthermore, QUIN or AA substantially reduced the histologic damage seen after 6-8 h in rabbit ileal segments. The cyclooxygenase inhibitor, indomethacin, also significantly inhibited (96%; n = 6) the secretory effects of toxin A in ligated rabbit intestinal segments. The destruction by toxin A of F-actin at the tight junctions of T-84 cell monolayers was not inhibited by AA or BPB. AA or QUIN had no effect on the T-84 cell tissue resistance reduction over 8-24 h after toxin A exposure. All the inhibitors were shown to be effective in the doses administered direct in ileal loops to inhibit PLA2 activity. The data suggest that PLA2 is involved in the major pathway of toxin A-induced histologic inflammatory damage and hemorrhagic fluid secretion.
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These findings support the hypothesis that the 20-HETE/CYP4A system modulates vessel responses to norepinephrine and vascular relaxation to reduced PO₂ in mesenteric resistance arteries of SS rats fed HS diet.
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From Jun. 2009 to Dec. 2011, we performed excision of ectopic ossification around the elbow in 78 stiff elbows. For each case, we used both medial and lateral approaches, and we performed both anterior and posterior capsulectomies and removal of ectopic ossification. In the lateral approach, we started proximally, the lateral supracondylar ridge of the humerus was exposed from the interval between extensor carpi radialis longus (ECRL) and triceps, and then distally passed the interval between ECRL and extensor carpi radialis brevis (ECRB). With the medial approach, after releasing the ulnar nerve, the pronator teres muscle origin was reflected from the medial epicondyle, and then the common flexor-pronator tendon was split longitudinally distally and the brachalis and the anterior portion of the flexor-pronator group were dissected off the anterior humerus. If there was forearm rotation dysfunction, we used extensive lateral approach, the anconeus muscle was reflected from the ulna and the scar tissue and ectopic ossification around the proximal radioulnar joint were resected. The important structures, such as the lateral ulnar collateral ligament (LUCL) and the anterior part of the medial collateral ligament (AMCL), should be carefully protected, because they were important for the elbow stability. Anterior transposition of the ulnar nerve depended on the patients' condition. We performed low dose radiotherapy 4 hours before operation, and we used indomethacin for 6 weeks after operation. In these patients, there were 46 males and 32 females, whose age averaged (35.8±7.9) years (16-65 years). According to Hastings-Graham classification, there were 56 IIA, 5 IIB, 6 IIC and 11 III before operation.
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A prospective clinical study was performed to compare the efficacy of low-molecular-weight heparin and indomethacin for the prevention of deep-vein thrombosis after total knee arthroplasty in Asian patients.
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We checked the hypothesis whether the non-classical estrogen receptor modulators genistein and raloxifene could affect platelet aggregation through their direct effect on vascular tissue by regulating the synthesis of vasoactive compounds. In rat aortic strips, 10nM genistein or 10nM raloxifene significantly increased nitric oxide synthesis, event prevented by ICI182780. Both agents exhibited an antiaggregatory action, dependent on the nitric oxide release from vascular tissue, since preincubation of aortic strips with L-NAME partially and completely suppressed the inhibition of platelet aggregation induced by genistein or raloxifene respectively. The phytoestrogen enhanced phospholipase A(2) and prostacyclin release into the incubation medium. Indomethacin reduced in half the inhibition of platelet aggregation elicited by genistein. Finally, genistein or raloxifene also inhibited platelet aggregation in aortic strips from ovariectomized rats. In conclusion, genistein and raloxifene exhibit an antiplatelet activity through their direct action on vascular tissue, in rats with or without ovarian activity.
At 1 month follow-up, both treatment arms resulted in increased range of motion and decreased pain. The steroid group decreased in active abduction while the NSAID group increased (steroid: 134°, NSAID: 151°, P = .03). The mean improvement in the UCLA shoulder rating scale at 4 weeks was 7.15 for the NSAID group and 2.13 for the steroid group (P = .03). Subgroup analysis of the UCLA scale demonstrated an increase in both forward flexion strength (P = .04) and patient satisfaction (P = .03) in the NSAID group. No significant difference could be seen in all other outcome measures.
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Consistent with earlier studies, medially situated SVZ cells expanded after H/I. Contrary to our expectations, indomethacin significantly decreased both the initial reactive increase in these precursors and their ability to self-renew. By contrast, indomethacin increased proliferation in the SGZ and lateral SVZ. Indomethacin diminished the accumulation of microglia/macrophages and IL-6 production after H/I. In vitro IL-6 enhanced neurosphere growth, self-renewal, and tripotentiality and was more effective than LIF in promoting self-renewal. Enhanced precursor self-renewal also was obtained using prostaglandin E2, which is downstream of cyclooxygenase 2 and a target of indomethacin.
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Leaf methanol extract of C. orbiculata L. was investigated for antinociceptive and anti-inflammatory activities using acetic acid writhing and hot-plate tests and carrageenan-induced oedema test in mice and rats, respectively. C. orbiculata (100-400 mg/kg, i.p.) significantly inhibited acetic acid-induced writhing and significantly delayed the reaction time of mice to the hot-plate-induced thermal stimulation. Paracetamol (300 mg/kg, i.p.) significantly inhibited the acetic acid-induced writhing in mice. Morphine (10 mg/kg, i.p.) significantly delayed the reaction time of mice to the thermal stimulation produced with hot plate. Leaf methanol extract of C. orbiculata (50-400 mg/kg, i.p.) significantly attenuated the carrageenan-induced rat paw oedema. Indomethacin (10 mg/kg, p.o.) also significantly attenuated the carrageenan-induced rat paw oedema. The LD(50) value obtained for the plant species was greater than 4000 mg/kg (p.o.). The data obtained indicate that C. orbiculata has antinociceptive and anti-inflammatory activities, justifying the folklore use of the plant species by traditional medicine practitioners in the treatment of painful and inflammatory conditions. The relatively high LD(50) obtained shows that C. orbiculata may be safe in or nontoxic to mice.