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Indocin (Indomethacin)
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Indocin

Indocin is an effective medication which helps to fight with pain or inflammation caused by many conditions such as gout, ankylosing spondylitis, arthritis, bursitis, or tendinitis. Indocin acts by reducing hormones that cause inflammation and pain in the body. It is nonsteroidal anti-inflammatory drug.

Other names for this medication:

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Also known as:  Indomethacin.

Description

Indocin is a perfect remedy, which helps to fight against pain or inflammation caused by many conditions such as gout, ankylosing spondylitis, arthritis, bursitis, or tendinitis.

Indocin acts by reducing hormones that cause inflammation and pain in the body.

Indocin is also known as Indometacin, Indocid, Inmecin, Indochron E-R, Indocin-SR, Flexin Continus, Indolar, Indomax, Indomod, Pardelprin, Rheumacin, Rimacid, Slo-Indo.

It is nonsteroidal anti-inflammatory drug.

Dosage

Shake the liquid form of Indocin before using.

Take Indocin tablets and liquid form orally with water.

Take Indocin once or twice a day at the same time.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Indocin suddenly.

Overdose

If you overdose Indocin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Indocin overdosage: vomiting, migraine, lightheadedness, confusion, extreme tiredness, feeling of numbness, pricking, burning, creeping on the skin, convulsions, dyspepsia.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Indocin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Indocin if you are allergic to Indocin components.

Do not take Indocin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Indocin if you are taking angiotensin ii receptor antagonists such as candesartan (atacand), eprosartan (teveten), irbesartan (avapro), losartan (cozaar), olmesartan (benicar), telmisartan (micardis), and valsartan (diovan); beta blockers such as atenolol (tenormin), labetalol (normodyne), metoprolol (lopressor, toprol xl), nadolol (corgard), and propranolol (inderal); cyclosporine (neoral, sandimmune); digoxin (lanoxin); diuretics ('water pills') such as triamterene (dyrenium, in dyazide); lithium (eskalith, lithobid); methotrexate (rheumatrex); phenytoin (dilantin); and probenecid (benemid), angiotensin-converting enzyme (ace) inhibitors such as benazepril (lotensin), captopril (capoten), enalapril (vasotec), fosinopril (monopril), lisinopril (prinivil, zestril), moexipril (univasc), perindopril (aceon), quinapril (accupril), ramipril (altace), and trandolapril (mavik).

It can be dangerous to use Indocin if you suffer from or have a history of seizures, parkinson's disease, depression or mental illness, or liver or kidney disease.

Be careful with Indocin if you are planning to use indomethacin suppositories.

Be careful with Indocin if you had proctitis (inflammation of the rectum) or have recently had rectal bleeding, asthma, frequent stuffed or runny nose or nasal polyps (swelling of the lining of the nose).

Avoid alcohol.

Be careful with Indocin if you are going to have a surgery.

Avoid driving machine.

Do not stop take it suddenly.

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Virodhamine, unlike WIN 55,212-2, relaxed 5-HT-precontracted vessels concentration dependently. The effect of virodhamine was reduced by endothelium denudation, two antagonists of the endothelial cannabinoid receptor, cannabidiol and O-1918, and a high concentration of the CB(1) receptor antagonist rimonabant (5 muM), but only slightly attenuated by the NOS inhibitor L-NAME and not affected by a lower concentration of rimonabant (100 nM) or by the CB(2) and vanilloid receptor antagonists SR 144528 and capsazepine, respectively. The COX inhibitor indomethacin and the fatty acid amide hydrolase inhibitor URB597 and combined administration of selective blockers of small (apamin) and intermediate and large (charybdotoxin) conductance Ca(2+)-activated K(+) channels attenuated virodhamine-induced relaxation. The vasorelaxant potency of virodhamine was lower in KCl- than in 5-HT-precontracted preparations.

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The present study was designed to establish whether penile dorsal arteries isolated from rabbits fed a high cholesterol diet show an enhanced contractile and/or impaired vasodilator response to histamine, and to characterize the histamine receptor subtype involved through in vitro isometric techniques. New Zealand White rabbits were fed a normal diet or a 1% cholesterol diet for 16 weeks. Arteries from cholesterol-fed rabbits retained the ability to relax in response to acetylcholine, whereas histamine and noradrenaline induced a greater contraction response compared to that observed in controls. In both groups, histamine-induced contraction was unaffected by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), its precursor L-arginine or the cyclooxygenase inhibitor indomethacin. Treatment of arterial rings in the control and hypercholesterolemia groups with the H1 receptor antagonist, mepyramine, unmasked a vasodilation response to histamine. This was followed by contraction at higher concentrations showing a leftward displacement of the histamine curve compared to controls. The histamine receptor that induced contraction in preparations from the hypercholesterolemic animals was of the H1 subtype, whereas the receptor involved in histamine-induced relaxation was H2. The affinity of histamine receptor agonists was comparable to their effects in control animals, and receptor antagonists showed the same potency in both groups. Our findings indicate a preserved endothelial function and enhanced contraction in response to histamine in penile dorsal arteries, probably due to a change in the sensitivity of the contractile machinery of smooth muscle but not a mechanism mediated by a receptor.

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The effect of three concentrations of safranal on histamine (H(1)) receptors was tested on two groups of tracheal chains incubated with: 1) indomethacin, and 2) indomethacin, propranolol and atropine (n = 6). The EC(50) (effective concentration of histamine causing 50% of maximum response) obtained in the presence of chlorpheniramine and all concentrations of safranal in both groups were significantly greater than those of saline (p < 0.05 to p < 0.001). The EC(50) obtained in the presence of all concentrations of safranal and maximum response of its two higher concentrations (1.25 and 2.5 μg/mL) in group 2 were greater than in group 1 (p < 0.05 to p < 0.001).

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Neonatal piglets were fed a liquid milk replacer and on day 3 of age infected or not with 10(8) C. parvum oocysts and the milk replacer supplemented with L-arginine or L-alanine. Milk consumption, body weight, fecal consistency, and oocyst excretion were recorded daily. On day 3 postinfection, piglets were euthanized and serum concentration of NO metabolites and histological severity of villous atrophy and epithelial infection were quantified. Sheets of ileal mucosa were mounted in Ussing chambers for measurement of barrier function (transepithelial resistance and permeability) and short-circuit current (an indirect measurement of Cl secretion in this tissue).

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Establishment, growth, and total burden of endometriotic lesions.

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Indomethacin chitosan nanoparticles (NPs) were developed by ionotropic gelation and optimized by concentrations of chitosan and tripolyphosphate (TPP) and stirring time by 3-factor 3-level Box-Behnken experimental design. Optimal concentration of chitosan (A) and TPP (B) were found 0.6mg/mL and 0.4mg/mL with 120min stirring time (C), with applied constraints of minimizing particle size (R1) and maximizing encapsulation efficiency (R2) and drug release (R3). Based on obtained 3D response surface plots, factors A, B and C were found to give synergistic effect on R1, while factor A has a negative impact on R2 and R3. Interaction of AB was negative on R1 and R2 but positive on R3. The factor AC was having synergistic effect on R1 and on R3, while the same combination had a negative effect on R2. The interaction BC was positive on the all responses. NPs were found in the size range of 321-675nm with zeta potentials (+25 to +32mV) after 6 months storage. Encapsulation, drug release, and content were in the range of 56-79%, 48-73% and 98-99%, respectively. In vitro drug release data were fitted in different kinetic models and pattern of drug release followed Higuchi-matrix type.

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The colon cancer cell line Caco-2, exhibiting a small intestinal phenotype starting as a crypt cell and differentiating to a villous phenotype, and RIE, a rat intestinal epithelial cell line, were employed. Indomethacin was added to differentiated the Caco-2 and RIE monolayer, and cell death was quantified by MTT assay and LDH release in the cell culture supernatant. Indomethacin-induced cell death was also qualified by fluorescent probes under the fluorescent microscope. As a functional study, the permeability of the Caco-2 monolayer was assessed by measuring transepithelial electrical resistance (TEER) and the flux of FITC-conjugated dextran across the monolayer. Indomethacin-induced reactive oxygen species production in Caco-2 and RIE was evaluated by redoxsensitive fluorogenic probes using a fluorometer. In some experiments, antioxidants were used to clarify the role of reactive oxygen species on indomethacin-induced Caco-2 cell death.

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Recent studies have suggested that passive or active immunization with anti-amyloid beta peptide (Abeta) antibodies may enhance microglial clearance of Abeta deposits from the brain. However, in a human clinical trial, several patients developed secondary inflammatory responses in brain that were sufficient to halt the study.

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Fifty-four New Zealand white rabbits received ketorolac (250 μg/0.05 mL) in one eye by a single intracameral injection (group A, n = 18), single intravitreal injection (group B, n = 18), and single suprachoroidal injection (group C, n = 18). Drug concentrations in the vitreous, retina-choroid (RC), and plasma were determined by the methods of high-performance liquid chromatography at 0.5, 1, 2, 4, 8, and 24 hours after injection. The concentrations in the opposite eyes were also investigated.

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Three hundred and ninety one VLBW infants were admitted; 310 survived to discharge. Ninety five were diagnosed with a PDA during their hospitalisations; 21 had a PDA at discharge (10 received indomethacin, 11 were never treated). Among these, mean gestational age was 28 weeks, mean birth weight was 998 g, and median duration of hospitalisation was 73 days. Two infants were discharged on oxygen, two on diuretics, and two on both. None had congestive heart failure, and none died during infancy. Spontaneous closure occurred in 18 of 21 infants at a median PMA of 48 weeks (range 34-76; interquartile range 46-56). Two infants had coil occlusion at 11 months of age. One patient had a PDA at 14 months of age.

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Twelve previously untreated patients with various head and neck cancers were treated by peritumoral injection of a combination of cytokines (Multikine), in addition to zinc sulfate, indomethacin, and a single dose of cyclophosphamide, which were administered systemically. Response was evaluated clinically and histopathologically. T-lymphocyte determinants were studied by fluorescence-activated cell sorter analysis (against controls).

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The HE was obtained by exhaustive extraction in Soxhlet apparatus. The chemical characterization of HE was performed by Electrospray Fourier transform ion cyclotron mass spectrometry (ESI FT-ICR MS) analysis. Mice were used for the evaluation of the gastroprotective activity. HE was analyzed in the HCl/ethanol, hypothermic restraint stress ulcer and acetic acid. In the investigation of the gastroprotective mechanisms of HE, were performed the amount of adhered gastric mucus, participation of the α2-adrenoceptor, nitric oxide (NO) and prostaglandins (PGs) using the HCl/ethanol-induced gastric mucosa lesion model.

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60 consecutive patients undergoing non-cemented THA were randomized into two groups in a double-blind and controlled study. During surgery, all patients received standardized pain treatment with LIA. Postoperatively, they were treated either with a solution of Ropivacain, Ketorolac, and Adrenaline (LINFA group) or placebo (placebo group) administered through a catheter to the hip 10 and 22 h after surgery. Pain score, opioid consumption, and length of stay (LOS) were evaluated.

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The study was carried out at the College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, over the period 1999 to 2000. Male wistar rats were randomly divided into 12-16 rats in each group. Edema was induced by subplantar injection of 0.1 ml of carrageenan (10 mg/ml) and the resulting edema volume was measured by plethysmograph, 3 hours after the injections. Saline of 0.9% (0.1 ml/100 g) was administered to the first group serving as control. The second and third groups received variable concentration of allopurinol (12.5, 25, 50 mg/kg) and tenoxicam (0.0625, 0.125, 0.25 mg/kg) 30 minutes before carrageenan injection. The fourth group received a combination of tenoxicam and allopurinol. Similar procedures were carried out with respect to diclofenac at 1.25, 2.5, 5.0 mg/kg and indomethacin at 0.25, 0.5, 1.0 mg/kg. The activities of the drugs were expressed as percentage inhibition of edema.

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Ketorolac was administered to nine female and three male shorthair domestic cats as an I/V bolus of 0.5 mg/kg after intubation, and 20 minutes prior to ovariectomy or orchiectomy. Intra-operative cardiorespiratory variables were monitored and blood samples were collected over 24 hours. Concentrations of ketorolac in serum were determined by high-performance liquid chromatography to establish pharmacokinetic parameters.

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We have shown that indomethacin has the potential to activate Ca2+/ calmodulin-dependent protein kinase II (CaMKII), regardless of cyclooxygenase (COX) inhibition. To understand the underlying mechanism, the present study investigated the effect of indomethacin on protein phosphatases such as protein phosphatase 1 (PP1), protein phosphatase 2A (PP2A), and protein tyrosine phosphatase 1B (PTP1B).

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We present a patient, a sixty-seven-year-old woman, who had refractory accumulation of synovial fluid in the knee joints with pustulotic arthro-osteitis for more than 10 years. Fifty ml of synovial fluid from her right knee contained 6,480 pg/ml of interleukin-8 (IL-8) and 15,000/mm3 of neutorophils. At first, she was treated with 400 mg/day of indomethacin farnesil (a prodrug that is converted to indomethacin after intestinal absorption) for 24 weeks. Although, the volume of synovial fluid in her right knee had decreased to 35 ml at the 16th week, it increased to 50 ml at the 24th week again. She was treated with Kampo medicine, Keishikajutsubuto (Guizhi-shu-fu-tang). In the present case, Keishikajutsubuto showed more therapeutic effect to pustulotic arthro-osteitis to reduce volume of synovial fluid to almost 0 ml, IL-8 concentration to 673 pg/ml and number of neutrophils to 660/mm3. Our data showed that Keishikajutsubuto might be suitable for this patient to regulate synovial fluid volume, reduce IL-8 concentration in synovial fluid, and block neutrophils migration to synovial fluid compared to indomethacin therapy.

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IMT-treated animals presented better renal function with less acute tubular necrosis and reduced ROS and MPO production. Moreover, the treatment was associated with lower expression of TNF-alpha, PGE(2), PGES, and t-bet and upregulation of HO-1 and IL-10. This profile was mirrored in serum, where inhibition of COXs significantly decreased interferon (IFN)-gamma, TNF-alpha, and IL-12 p70 and upregulated IL-10.

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Seventeen preterm infants and 13 term infants had MRIs performed. There was no significant difference in weight and length at the time of MRI (p = 0.76 and 0.11, respectively). There was no significant difference in total renal volume or total kidney volume to weight ratio between the preterm and term neonates (p = 0.83 and 0.6, respectively).

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Our results highlight to the existence of a complex interaction between pulmonary allergy and gastric juice in the airways. The involvement of the non-adrenergic non-cholinergic system, NO, prostanoids and mast cells are directly related to this interaction. We suggest that the reduced contractile response observed in vitro may represent a protector mechanism of the airways. Despite its presence in the human body it can not be observed due to the predominant effects of excitatory the non-adrenergic non-cholinergic system.

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The death of chondrocytes by apoptosis is characteristic of degenerative joint diseases, such as osteoarthritis (OA). Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) have been shown to play an important role in the development of OA. In this study we analyzed the effects of TNF-alpha and IL-1beta on cell death in normal human chondrocytes.

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An English-language literature review was conducted using the PubMed database in November 2007. In compiling evidence on current management trends of ICP and FHF, the paired keywords: fulminant hepatic failure and either mannitol, hypertonic saline, hyperventilation, bioartificial liver, hypothermia, indomethacin, thiopental, or propofol were used. In compiling evidence on ICP monitoring in FHF, the terms "intracranial pressure monitoring" and "liver failure" were used. Excluded references were either pertinent to animal research or irrelevant to ICP monitoring and ICH management in the setting of FHF.

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indocin and alcohol 2017-01-19

Water channel AQP2 is the target for vasopressin (AVP) and a major determinant of urinary concentrating capacity. In mature kidneys, prostaglandins counteract the effect of AVP on AQP2 expression at functional sites. We investigated whether disturbances in water homeostasis in infants with patent ductus buy indocin arteriosus (PDA) treated with prostaglandin inhibitors can be attributed to activation of AQP2.

indocin name brand 2015-09-21

The results of the buy indocin first model showed an ulcer inhibition of 60,4% and 66,7% using the doses of Capsicum at 10 mg/kg and 100 mg/kg, respectively. The results of the second model showed that neither the pH nor the volume of the gastric content were modified by the administered extract (p >0.05); however, by using the doses of Capsicum at 100 mg/kg and 1000 mg/kg, there was clearly an ulcer inhibition of 75.59% and 81.63% respectively, which were even greater than the inhibition obtained by ranitidine (75.51%).

indocin gel 2015-05-02

Forty Wistar albino rats of which the weights ranged between 310 and 370 g were included in this study. Middle ear effusion was created by transtympanic histamine injection. The presence of effusion was confirmed by otomicroscopic examination. Thirty-seven rats with effusion were divided into 4 groups (methylprednisolone, montelukast, indomethacine and saline-control groups). All agents were administered for a period of consecutive 10 days. At the 11th days of administration, the recovery buy indocin of effusion was confirmed by otomicroscopic examination. Tympanic bullae of the rats were removed and histopathological examinations were carried out. In the histopathological examination, the neutrophil leukocytes accumulated in the middle ear submucosa were counted.

indocin tab 2017-05-21

Avoidance of the nicotine withdrawal syndrome as well as the positive subjective effects of nicotine is the major predisposing factor to motivate nicotine abuse. However, its underlying neurobehavioral mechanisms remain perplexing. In the present study, we investigated the influence of the neurosteroid allopregnanolone (ALLO; 0.5-2mg/kg) on the development of nicotine withdrawal in mice. Chronic nicotine injections buy indocin (2mg/kg, four times daily, 10 days) followed by its withdrawal, elicited severe somatic signs, anxiety and marked reduction in locomotion. However, these withdrawal signs were not evident in animals pretreated with ALLO or progesterone (Day 8-10) daily before 1st injection of nicotine. This effect of neurosteroid on the nicotine withdrawal signs was reversed by indomethacin and finasteride the inhibitors of neurosteroid biosynthesis. On the contrary, single or repeated dose administration of ALLO or progesterone during nicotine withdrawal (Day 11) did not affect the expression of nicotine withdrawal signs. Thus, compounds that modulate endogenous neurosteroid ALLO are likely to have therapeutic potential for treating various aspects of nicotine dependence and withdrawal.

indocin purchase 2017-01-09

MEDLINE, Scopus and ISI Web of Knowledge databases, using the following medical subject headings and terms: paracetamol, acetaminophen and patent ductus arteriosus. Electronic and manual screening of conference abstracts from international meetings of relevant organisations. Manual search of the reference lists of all eligible buy indocin articles.

indocin dosage chart 2015-01-17

This was a randomized-sequence, open-label, single-dose, 2-period crossover (2 dosing periods x 2 treatments) study comparing the bioavailability of two 30-mg sublingual tablet formulations of ketorolac. Healthy Mexican adult (aged, 18-55 years) men and women were eligible for inclusion. Subjects were randomly assigned in a 1:1 ratio to receive a single dose of the test formulation or the reference formulation. After a 12-hour overnight fast, subjects received a single dose of the corresponding formulation. There was a 7-day washout period between administration periods. Plasma samples were obtained over a 24-hour period after administration. Plasma ketorolac concentrations were analyzed by high-performance liquid chromatography for analysis of pharmacokinetic properties, including Cmax, AUC0-24, and AUC0-infinity. Blood samples were drawn immediately after sublingual placement of the drug and at 10, 20, 30, 40, 50, 60, 75, and 90 minutes and 2, 4, 6, 8, 10, 12, and 24 hours after dosing. The formulations were considered bioequivalent if the geometric mean ratios of Cmax and AUC were within the predetermined range of 80% to 125% and if P for the buy indocin 90% CIs was <0.05. Tolerability was assessed by vital sign monitoring, laboratory analysis results, and subject interviews.

indocin tablets uses 2016-11-16

Epidemiological studies have shown that use of non-steroidal anti-inflammatory drugs (NSAIDs) by the elderly is associated with a decreased relative risk and a delayed onset of Alzheimer's disease (AD). In contrast, the apolipoprotein E (apoE) gene has proven to be a risk factor for AD with apoE epsilon 4 AD patients having been found to show lower levels of brain apoE. In the present study, treatment of primary rat mixed glial cell cultures with the common NSAIDs, indomethacin and aspirin, induced significant increases in extracellular apoE protein levels. Similarly, treatment of primary rat astrocyte cell cultures with aspirin and a cyclooxygenase (COX)-2-selective aspirin derivative also stimulated significant increases in apoE protein. However, astrocyte and mixed glial apoE protein levels were significantly reduced following exposure to COX-2-specific indomethacin amides and an inactive indomethacin derivative. ApoE protein modulation was observed at physiological and subphysiological concentrations well below the COX inhibition IC50 values of the NSAIDs used, suggestive of a COX-independent mechanism. In contrast to these results, indomethacin and aspirin treatment failed to induce any significant changes in apoE mRNA levels. The failure of NSAIDs to buy indocin significantly alter apoE expression may have been indicative of a nontranscriptional mechanism of apoE protein induction. Consequently, NSAID-induced increases in apoE protein may enhance apoE-mediated immunosuppression and compensatory synaptic plasticity, potentially resulting in decreased AD risk and delay of disease onset.

indocin sr alcohol 2016-07-23

In the gastric epithelium in buy indocin vivo, TFFs promote epithelial restitution via a mechanism that does not require cyclooxygenase activation. A novel role for TFFs to affect gastric surface pH is observed.

indocin pill 2015-03-09

The incidence of patent ductus arteriosus (PDA) in premature neonates varies according to the gestational age and respiratory status. Failure of PDA closure in preterm infants with respiratory distress syndrome results in a left to right shunt across the duct which may lead to pulmonary congestion and deterioration in respiratory buy indocin status. Although indomethacin and ibuprofen are the main stay of medical treatment, conservative approach by restricted fluid and applying continuous positive airway pressure (CPAP) may be effective in prevention of PDA without complication. The daily clinical round debate on how to diagnose, when, and how to treat PDA in preterm neonates will be discussed with details in this review.

indocin medication generic 2016-09-10

Akt has been reported to suppress p27(Kip1) promoter activity through Forkhead box O (FOXO) in different kinds of cells. Previous studies indicated that anti-inflammatory drugs up-regulated p27(Kip1), and this effect might play an important role in anti-inflammatory drug-induced cell cycle arrest of buy indocin human osteoblasts (hOBs). In this study, we hypothesized that these drugs might increase p27(Kip1) expression in hOBs by altering the Akt/FOXO signaling. We tested this hypothesis by examining the influences of three anti-inflammatory drugs on the levels and/or activities of Akt, FOXO and p27(Kip1) as well as the relationship between these factors and proliferation of hOBs. We tested the effects of indomethacin (10(-5) and 10(-4)M), celecoxib (10(-6) and 10(-5)M), and dexamethasone (10(-7) and 10(-6)M) using PI3K inhibitor, LY294002 (10(-5)M) as the basis of comparison. The three drugs suppressed the canonical level of phosphorylated Akt in hOBs. This was accompanied by elevated FOXO3a level and increased promoter activity, mRNA expression and protein level of p27(Kip1). Furthermore, the anti-inflammatory drugs suppressed the EGF-induced increases in proliferation, phosphorylation, and nucleus translocation of Akt. Simultaneously, they suppressed EGF-induced decreases of FOXO3a nucleus accumulation and p27(Kip1) mRNA expression. On the other hand, FOXO silencing significantly attenuated the drug-induced up-regulation of p27(Kip1) and suppression of proliferation in hOBs. To the best of our knowledge, this study represents the first to demonstrate that Akt/FOXO3a/p27(Kip1) pathway contributes to suppression of hOB proliferation by anti-inflammatory drugs. We suggest that anti-inflammatory drugs suppress hOB proliferation, at least partly, through inactivating Akt, activating FOXO3a, and eventually up-regulating p27(Kip1) expression.

indocin gout dosage 2017-12-16

Systemic inflammation may affect the brain by aggravating the stage of encephalopathy and increasing intracranial pressure (ICP) especially if liver insufficiency with hyperammonemia is present. The aim of this study was to determine if the influence of concomitant hyperammonemia and lipopolysaccharide (LPS) on the brain can be prevented by dexamethasone buy indocin and cyclooxygenase (COX) inhibitors.

indocin drug interactions 2016-06-09

Identification of protein targets of bioactive small molecules has been a technical hurdle of chemical genetics. Here we report a polyproline-rod approach to isolating protein targets of small molecules from cell lysates. buy indocin The results indicate that insertion of a long, rigid polyproline helix between a small-molecule bait and a biotin tag boosts the capacity of affinity purification and thereby permits isolation of low-abundance or low-affinity proteins. In the course of the proof-of-concept experiments, we isolated glyoxalase 1 (GLO1) as a new target of indomethacin, a widely used antiinflammatory drug. Molecular biological experiments suggest that inhibition of GLO1 enzyme activity is related to the clinically recognized beneficial side effects of the indomethacin family of nonsteroidal antiinflammatory drugs.

indocin dosage 2017-02-03

Chantaleela recipe is buy indocin indicated for relieving fever in Thai traditional folk medicine. In the present study, Chantaleela recipe was investigated for anti-inflammatory, analgesic, antipyretic and anti-ulcerogenic activities. In preliminary investigation Chantaleela recipe was found to exert an inhibitory activity on the acute phase of inflammation as seen in ethyl phenylpropiolate-induced ear edema as well as in carrageenan-induced hind paw edema in rats. The results suggest that the anti-inflammatory activity of Chantaleela recipe may be due to an inhibition via cyclooxygenase pathway. In the analgesic test, Chantaleela recipe showed a significant analgesic activity in both the early and late phases of formalin test, but exerted the most pronounced effect in the late phase. The analgesic activity of Chantaleela recipe may act via mechanism at peripheral and partly central nervous system. In antipyretic test, Chantaleela recipe significantly decreased rectal temperature of brewer's yeast-induced hyperthermia rats, probably by inhibiting synthesis and/or release of prostaglandin E₂ in the hypothalamus. Therefore, the key mechanism of anti-inflammatory, analgesic, and antipyretic activity of the Chantaleela recipe likely involves the inhibition of the synthesis and/or release of inflammatory or pain mediators, especially prostaglandins. The oral administration of the Chantaleela recipe reduced ulcer formation in acute gastric ulcer models (EtOH/HCl-, indomethacin-, and stress-induced gastric lesions). In contrast, this recipe did not reduce the secretory rate, total acidity, and increase pH in rat stomach. These results indicated that Chantaleela seem to possess anti-ulcerogenic effect. This activity may be due to the increase of gastric mucosal resistance or potentiation of defensive factors and/or the decrease of aggressive factors but did not associate the anti-secretory activity. Moreover, the high oral doses treated did not cause acute toxicity in rats and the long term oral administration did not produce gastric and ileum lesions.

indocin reviews 2017-03-19

Condensation of 2-acetyltetralin with ethylcyanoacetate and/or malononitrile and some aldehydes in the presence of excess of ammonium acetate afforded the respective hydroxycyanopyridines or aminocyanopyridines 1a-f buy indocin and 2a-f. Treatment of 2-acetyltetralin with some sulfonylhydrazides yielded the hydrazone derivatives 3a-d, respectively, which upon treatment with thioglycolic acid gave the corresponding thiazole derivatives 4a-d, respectively. Compounds 4a-d underwent cyclocondensation with different arylidene derivatives to give the corresponding pyrane derivatives 5a-d. Upon the reaction of compounds 4a-d with some secondary amines and paraformaldehyde the corresponding Mannich bases 6a,c, 7b,d and 8a,d were obtained. Compounds 1c, 1d, 1e, 2e, 3a and 3d were evaluated as analgesic, anti-iflammatory and antipyretic agents.

indocin renal dosing 2016-08-31

We here present the case of a patient with headache and radiological findings of crowned dens. However, the clinical presentation differed from previous CDS cases in the literature in that the pain was unilateral with frontal localization and throbbing quality, as well as an orthostatic component and lack of either fever or inflammatory signs. The differential diagnosis also includes a remitting form Prograf Pediatric Dose of hemicrania continua, presenting with an atypical presentation, with neuroimaging incidental finding of CDS.

indocin dosage forms 2017-05-24

Between January 2005 and June 2009, a retrospective analysis was performed in preterm infants with a hemodynamically significant PDA (PDA group, n=72) and preterm infants without Valtrex Shingles Dose a PDA (control group, n=72) at the Chonnam National University Hospital Neonatal Intensive Care Unit. The PDA was closed by treatment with indomethacin. The BP was compared between the two groups over the seven days after the first dose of indomethacin.

indocin 40 mg 2016-03-12

Nonsteroidal anti-inflammatory drugs (NSAIDs), which are globally prescribed, exhibit mainly anti-inflammatory and analgesic effects but also can cause adverse effects including gastrointestinal erosions, ulceration, bleeding, and perforation. The purpose of this study was to investigate surrogate biomarkers associated with the gastrointestinal (GI) damage caused by NSAID treatment using pattern recognition analysis of (1)H-nuclear magnetic resonance ((1)H NMR) spectra of rat urine. Urine was collected for 5h after oral administration of the following NSAIDs at low or high doses: acetylsalicylic acid (10 or 200mgkg(-1)), diclofenac (0.5 or 15mgkg(-1)), piroxicam (1 or 10mgkg(-1)), indomethacin (1 or 25mgkg(-1)), or ibuprofen (10, or 150mgkg(-1)) as nonselective COX inhibitors and celecoxib (10 or 100mgkg(-1)) as a COX-2 selective inhibitor. The urine was analyzed using 500MHz (1)H NMR for spectral binning and targeted profiling and the level of gastric damage was examined. The nonselective COX inhibitors caused severe gastric damage Antabuse Pill while no lesions were observed in the celecoxib-treated rats. The (1)H NMR urine spectra were divided into spectral bins (0.04ppm) for global profiling, and a total of 44 endogenous metabolites were assigned for targeted profiling. Multivariate data analyses were performed to recognize the spectral pattern of endogenous metabolites related to NSAIDs using partial least square-discrimination analysis (PLS-DA). The (1)H NMR spectra clustered differently according to gastric damage score in global profiling. In targeted profiling, the endogenous metabolites of citrate, allantoin, 2-oxoglutarate, acetate, benzoate, glycine, and trimethylamine N-oxide were selected as putative biomarkers for gastric damage caused by NSAIDs. These putative biomarkers might be useful for predicting the risk of adverse effects caused by NSAIDs in the early stage of drug development process.

indocin 50 mg 2015-11-27

A retrospective chart review was performed. The exposure of interest was postoperative use of ketorolac after congenital heart surgery in infants and children. The outcome measured was postoperative bleeding requiring surgical exploration. The patients who received ketorolac were compared with an age- and diagnosis-matched comparison group who did not Famvir Drug receive ketorolac.

indocin er dosage 2017-07-29

Bilateral myringotomy and tympanostomy tube placement (BMT) is one of the most frequently performed pediatric outpatient procedures with 667,000 children receiving Zyrtec 20 Mg tympanostomy tubes annually. Because of this high volume, discovering the ideal analgesic regimen may lead to decreased overall postanesthesia care unit (PACU) costs while increasing patient and parent satisfaction. The purpose of this study is to determine if there is any benefit in supplementing intranasal (IN) fentanyl with intramuscular (IM) ketorolac with regard to immediate recovery characteristics.

indocin max dosage 2015-03-30

Neutrophil migration into tissues is involved in the genesis of inflammatory pain. Here, we addressed the hypothesis that the effect of CXC chemokines on CXCR1/2 is important to induce Cefixime Suspension neutrophil migration and inflammatory hypernociception.

indocin tablets dosage 2016-05-30

KRGCD (100 and 300 mg/kg, p.o.) significantly decreased ethanol- and indomethacin-induced gastric ulcer compared with the vehicle-treated (control) group. KRGCD (100 and 300 mg/kg) also decreased the level of thiobarbituric acid reactive substance (TBARS) and increased gastric mucosal blood flow compared with the control group.