Six weeks following surgery, rats were divided randomly into the following groups: a sham group, a model group, an MHBFC 12 mg/kg/day group (MHBFC 12), an indomethacin 2 mg/kg/day group (Indo 2), and an Indo 2+ MHBFC 12 group. The MS 4000 organism signal system was used to record the rats' hemodynamic indices. Additionally, the heart weight was determined, and the cardiac remodeling index was calculated. HE and Masson's stains were utilized to perform histological analyses; the immunofluorescence was used to observe the microvessel density of myocardial tissue; the colorimetric method was used to determine the hydroxyproline content of cardiac tissue; the ELISA method was used to measure the plasma PGI2 content; and transmission electron microscopy was used to observe the ultrastructure of the myocardium.
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This paper reports a new MEPS-HPLC-PDA method for the simultaneous analysis of seven non-steroidal anti-inflammatory drugs (Furprofen, Indoprofen, Ketoprofen, Fenbufen, Flurbiprofen, Indomethacin, and Ibuprofen) in human plasma and urine. NSAIDs were resolved on a Gemini C18 column (4.6 mm × 250 mm; 5 μm particle size) using a gradient elution mode with a run time of 25 min, comprising re-equilibration, without further purification. The method was validated over the concentration range from 0.1 to 10 μg/mL for all the analytes both in human plasma and urine, using Benzyl 4-hydroxybenzoate as the internal standards. This method was successfully tested to NSAIDs analyses in real matrices, in order to check the method potentiality and the correct response. The results from assay validations show that the method is selective, sensitive and robust. The limit of quantification of the method was 0.1 μg/mL for all analytes, and weighted-matrix-matched standard curves showed a good linearity up to 10 μg/mL. In order to check the correct response for over-range samples, parallelism tests were also assessed. In the entire analytical range the intra and inter-day precision (RSD%) values were ≤ 7.31% and ≤ 13.5%, respectively. For all the analytes the intra and inter-day trueness (Bias%) values ranged from -11.3% to 10.2%. To our knowledge, this is the first MEPS-HPLC-PDA based method that uses MEPS procedure for simultaneous determination of these seven NSAIDs in plasma and urine samples.
Effects of leucine and related compounds on protein synthesis were studied in L6 myotubes. The incorporation of [(3)H]tyrosine into cellular protein was measured as an index of protein synthesis. In leucine-depleted L6 myotubes, leucine and its keto acid, alpha-ketoisocaproic acid (KIC), stimulated protein synthesis, while D-leucine did not. Mepacrine, an inhibitor of both phospholipases A(2) and C, canceled stimulatory actions of L-leucine and KIC on protein synthesis. Neither indomethacin, an inhibitor of cyclooxygenase, nor caffeic acid, an inhibitor of lipoxygenase, diminished their stimulatory actions, suggesting no involvement of arachidonic acid metabolism. Conversely, 1-O-hexadecyl-2-O-methylglycerol, an inhibitor of proteinkinase C, significantly canceled the stimulatory actions of L-leucine and KIC on protein synthesis, suggesting an involvement of phosphatidylinositol degradation and activation of protein kinase C. L-Leucine caused a rapid activation of protein kinase C in both cytosol and membrane fractions of the cells. These results strongly suggest that both L-leucine and KIC stimulate protein synthesis in L6 myotubes through activation of phospholipase C and protein kinase C.
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The release of reactive oxygen specie (ROS) by activated neutrophil is involved in both the antimicrobial and deleterious effects in chronic inflammation. The objective of the present investigation was to determine the effect of therapeutic plasma concentrations of non-steroidal anti-inflammatory drugs (NSAIDs) on the production of ROS by stimulated rat neutrophils. Diclofenac (3.6 microM), indomethacin (12 microM), naproxen (160 microM), piroxicam (13 microM), and tenoxicam (30 microM) were incubated at 37 masculineC in PBS (10 mM), pH 7.4, for 30 min with rat neutrophils (1 x 10(6) cells/ml) stimulated by phorbol-12-myristate-13-acetate (100 nM). The ROS production was measured by luminol and lucigenin-dependent chemiluminescence. Except for naproxen, NSAIDs reduced ROS production: 58 +/- 2% diclofenac, 90 +/- 2% indomethacin, 33 +/- 3% piroxicam, and 45 +/- 6% tenoxicam (N = 6). For the lucigenin assay, naproxen, piroxicam and tenoxicam were ineffective. For indomethacin the inhibition was 52 +/- 5% and diclofenac showed amplification in the light emission of 181 +/- 60% (N = 6). Using the myeloperoxidase (MPO)/H2O2/luminol system, the effects of NSAIDs on MPO activity were also screened. We found that NSAIDs inhibited both the peroxidation and chlorinating activity of MPO as follows: diclofenac (36 +/- 10, 45 +/- 3%), indomethacin (97 +/- 2, 100 +/- 1%), naproxen (56 +/- 8, 76 +/- 3%), piroxicam (77 +/- 5, 99 +/- 1%), and tenoxicam (90 +/- 2, 100 +/- 1%), respectively (N = 3). These results show that therapeutic levels of NSAIDs are able to suppress the oxygen-dependent antimicrobial or oxidative functions of neutrophils by inhibiting the generation of hypochlorous acid.
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Intravenous migraine therapy reduces PTH pain scores for children presenting within 14 days after mTBI. Further prospective work is needed to determine long-term benefits of acute PTH treatment in the ED.
The leaf extract of Sedum dendroideum exhibited gastroprotective activity, potentially due to sulfhydryl compounds and antioxidant activity. Therefore, other studies are warranted to elucidate the antiulcer properties of these compounds.
A head to head comparison study on renal function and ductal response between indomethacin and ibuprofen has rarely been conducted in extremely low birth weight (ELBW) infants.
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The ethanolic extract and its fractions were given at a dose of 200 mg/kg po and 300 mg/kg po for testing their anti-inflammatory activity by carrageenan induced hind paw edema. The analgesic activity of the ethanolic extract and its fractions has been carried out by tail-flick method and writhing test at a dosage of 300 mg/kg po. Gastric ulceration studies have been further carried out to study the antiulcer effect of the ethanolic extract and its various fractions at dose of 900 mg/kg body weight.
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The present study was aimed to evaluate the effect of licofelone, a dual inhibitor of cycloxygenase1/2-5-lipoxygenase against indomethacin-induced gastric damage in rats and mice in order to assess the role of leukotrienes if any, in non-steroidal anti-inflammatory drugs (NSAIDs)-induced gastrointestinal inflammation. Acute pretreatment with licofelone reversed the indomethacin-induced gastric ulceration, neutrophil adhesion in mesentery venules, neutrophil count in blood, lipid peroxides and vascularity in the stomachs of mice and rats. Further, chronic pretreatment of licofelone also prevented indomethacin-induced gastric morphological changes and cellular infiltration in mesentery venules. Moreover, acute administration of indomethacin elevated leukotriene B4 levels in gastric mucosa, which was reversed by pretreatment with licofelone The results suggest that licofelone offered gastroprotection against NSAIDs-induced gastropathy through its effect on leukotrienes and by inhibiting extravasation of neutrophils.
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A series of blends of polydimethylsiloxane (PDMS) and indomethacin (IMC), containing 20-80 wt.% IMC were obtained and characterized by differential scanning calorimetry, Fourier transform-infrared spectroscopy, and powder X-ray diffraction in order to observe the mutual influence of the two components. The main thermal transitions of PDMS remained un-changed. Both the solvent (tetrahydrofuran, THF) and the PDMS influenced the crystalline form of IMC. The blends were subsequently re-dissolved in THF, with or without cross-linking reagents added and precipitated into diluted aqueous solutions of siloxane-based surfactants. The resulted nanoparticles were analyzed by dynamic light scattering and scanning electron microscopy. Most of the particles had diameters between 200 and 300 nm. The surfactants, the IMC content and the cross-linking influenced the particles size and polydispersity, as well as the nanoparticle yield. The maximum drug release from selected aqueous formulations was 30%.
Anti-nociceptive and anti-inflammatory effects of methanolic extract of Wrightia arborea (MEWA) were examined using different models in rats. MEWA was given to rats orally upto 2000 mg kg(-1) b.wt. for acute toxicity study and observed for 14 days. Anti-nociceptive activity was evaluated in rats against Acetic acid induced writhing (chemically induced pain) and Tail immersion method (thermally induced pain). Acute anti-inflammatory activity of MEWA was also evaluated in Formaline-induced rat paw edema model and Carrageenan-induced hind paw edema model in rats. Results demonstrated that no mortality was found upto single dose of 2000 mg kg(-1) b.wt. in rats even after 14 days observation. In comparison to control group MEWA at 100 and 200 mg kg(-1) b.wt. showed highly significant anti-nociceptive activity against chemically (p < 0.001) as well as thermally (p < 0.05 and p < 0.001) induced pain as compared to standard drugs, indomethacin and nalbufin, respectively. In the formalin test, both the doses of 100 and 200 mg kg(-1) of extract significantly prevented increase in volume of paw edema (p < 0.05 and p < 0.01) both in the neurogenic and inflammatory phases. MEWA (200 and 400 mg kg(-1) p.o.) also significantly prevented increase in volume of paw edema in Carrageenan test (p < 0.05 and p < 0.001). The results suggest that MEWA has significant analgesic and anti-inflammatory potential which may be mediated by central and peripheral mechanism.
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The objective of this work was to investigate the influence of various micronized poorly water-soluble inorganic materials on the dissolution and de-agglomeration behaviour of a micronized, poorly water-soluble model drug, indomethacin, from lactose interactive mixtures. Dissolution of indomethacin was studied using the USP paddle method and the data were modelled with multi-exponential equations using a nonlinear least squares algorithm in order to obtain key parameter estimates. The dispersion of indomethacin mixtures was measured by laser diffraction. The addition of aluminium hydroxide and calcium phosphate to binary mixtures of indomethacin counter-intuitively improved the dissolution rate of indomethacin due to significant increases in both the estimated initial concentration and dissolution rate constant of dispersed particles of indomethacin. While some enhancement was due to pH changes in the dissolution medium, the presence of these poorly water-soluble inorganic salts caused de-agglomeration. Average particle size distributions indicated that the presence of aluminium hydroxide within the matrix of indomethacin had reduced the agglomerate concentration whilst increasing the dispersed particle concentration. These findings provide the first evidence of the ability of poorly water-soluble inorganic salts to enhance the de-agglomeration and dissolution of micronized powders, potentially translating to improved bioavailability of poorly water-soluble drugs.
Inflammation promotes epidermal wound healing but is considered detrimental to recovery from central nervous system injury. Sick infants have increased levels of cytokines in their cerebrospinal fluid that correlate with poor neurological outcome. In this study, we investigated the role of neuroinflammation and more specifically interleukin 6 (IL-6) in the amplification of subventricular zone (SVZ) and subgranular zone (SGZ) neural precursors after neonatal brain injury.
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The aim of this study was to evaluate and compare the permeation of model drug indomethacin (IND) from various types of gels through several semipermeable membranes.
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BNP-guided treatment reduced the number of primary indomethacin doses. There was no increase in PDA persistence or associated morbidity.
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Indomethacin or placebo intravenously once daily for the first 3 days.
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Carotid endarterectomy (CEA) and more recently carotid artery stenting are the treatments of choice for atherosclerotic disease of the extracranial carotid arteries; however, early restenosis caused by neointimal hyperplasia confounds surgical therapy. Oxidative stress has been implicated in the progression of intimal hyperplasia. The authors hypothesized that ketorolac tromethamine (Toradol), a nonsteroidal antiinflammatory drug that is a potent cyclooxygenase inhibitor, would decrease oxidative stress and thereby reduce intimal hyperplasia in a rat CEA model. Twenty-nine male Sprague-Dawley rats underwent CEA and were divided into 3 treatment groups as follows: (1) control (placebo), (2) 7.5 mg/kg Toradol, and (3) 10 mg/kg Toradol. Toradol treatment began 2 days before CEA and continued for 2 weeks. Two weeks after endarterectomy, carotid arteries were fixed, harvested, and examined for platelet activity (platelet reactive units), oxidative stress (malondialdehyde and glutathione), and intimal hyperplasia (measured as percentage of luminal stenosis). Platelet activity, malondialdehyde and glutathione, and intimal hyperplasia were all significantly lowered in both 7.5- and 10-mg/kg doses of Toradol versus control. Toradol given daily beginning 2 days before CEA and ending 2 weeks after the procedure was effective at significantly reducing platelet activity, oxidative stress, and intimal hyperplasia development in the rat without any increase in bleeding. Although the mechanism of action of this reduction is not completely understood, one possible explanation may be through the inhibition of reactive oxygen species production.
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Angiotensin II (AngII) is important in regulation of vascular resistance and control of blood flow among organs and tissues. The effect of AngII on the cerebral microvasculature may be mediated or altered by endothelial-derived signals. The aim of this study was to test the hypothesis that blood AngII dilates neonatal pial arterioles via an endothelial-dependent mechanism but brain AngII can constrict pial arterioles by activating smooth muscle AT1 receptors. Studies used anesthetized newborn pigs with surgically implanted closed cranial windows. AngII was given either by infusion into the carotid artery ipsilateral to the cranial window or topically. Intracarotid infusion of AngII dilated pial arterioles. The dilation was blocked by systemic administration of the AT1-receptor antagonist, losartan, but unaffected by topical losartan. Topical AngII also caused dilation, but this dilation was converted to constriction by topical losartan. In piglets pretreated with the angiotensin-converting enzyme (ACE) inhibitor, enalapril, topical AngII constricted, rather than dilated, pial arterioles. In enalapril-treated piglets, light/dye endothelial injury blocked dilation to intracarotid AngII but did not affect constriction to topical AngII. Either indomethacin or l-nitroarginine methyl ester blocked the dilation to intraluminal AngII, but neither affected constriction to topical AngII. Chromium mesoporphyrin, that inhibits heme oxygenase, did not affect responses to either topical or intravascular AngII. These data are consistent with the hypotheses that: (a) circulating AngII dilates pial arterioles via endothelial AT(1) receptor-derived relaxing factors, notably prostanoids and nitric oxide; (b) direct AT(1) receptor activation on the brain side of the blood-brain barrier by AngII causes AT(1) receptor-mediated constriction that can mask underlying AT(1) receptor-independent dilation when ACE is inhibited. Clinical manipulation of the renin-angiotensin system will have disparate actions on cerebral circulation depending on the functional integrity of the intima and ACE.
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RAS inhibitors combined with indomethacin showed beneficial effect in our patient. Thus, this combination might be the initial treatment of patients with FS. If this treatment strategy was not satisfied for at least 3 months, then CsA would be considered to be administered taking account of the nephrotoxicity and the increased risk of malignancy. Further prospective study is required to clarify this issue.
The present investigation provides evidence for the decreased responsiveness to both, ACh-endothelium-dependent and VIP-endothelium-independent vasorelaxation in rabbit facial artery after carotid occlusion. In addition, the data suggest that ischaemia alters contribution of endothelial nitric oxide (eNO) and prostaglandin to ACh, and vascular smooth muscle's cAMP and neuronal NO to VIP vasorelaxant effects.
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ELBW Infants that acquire SIP were more likely to have been exposed to early indomethacin and post-natal glucocorticoids. However, no association was found between SIP and ANS within a well-powered cohort.
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The ketorolac group consisted of 94 patients (100 eyes) and the nepafenac group, 89 patients (93 eyes). The between-group differences in visual outcomes and anterior chamber inflammation were not statistically significant (mean P = .33). There was a higher incidence of posterior capsule opacification in the nepafenac group (P = 0.019). Patient satisfaction, patient compliance, and postoperative pain control were statistically significantly better in the ketorolac group (P = .022, P = .023, and P = .025, respectively).
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After laparoscopic cholecystectomy under general anesthesia using intravenous propofol, nitrous oxide and fentanyl 3 micrograms.kg-1, 40 patients were randomly allocated to receive either intravenous flurbprofen 50 mg or suppository indomethacin 50 mg. Visual analogue scales of postoperative pain at 0, 10, 20, 30 and 60 min after surgery (at rest and at coughing), use of rescue analgesics, and the presence or absence of complications were recorded.
EP4-selective agonist may prevent indomethacin-induced gastric lesions and promote healing of existing and indomethacin-aggravated gastric ulcers, via promoting proliferation and survival of mucous epithelial cells.
Frequency and severity of the blunt chest injuries are increasing. Rather high letality is caused by the injury and following systemic inflammatory response.