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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.

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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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Topical ketorolac was well tolerated and safe, reduced postoperative pain and inflammation, and improved visual recovery in this prospective, double-masked trial.

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80 patients undergoing elective THA under spinal block were randomly assigned to receive either (1) continuous epidural infusion (group E) or (2) infiltration around the hip joint with a mixture of 100 mL ropivacaine 2 mg/mL, 1 mL ketorolac 30 mg/mL, and 1 mL epinephrine 0.5 mg/mL at the conclusion of surgery combined with one postoperative intraarticular injection of the same substances through an intraarticular catheter (group A).

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Vaginal indomethacin is more effective than oral for prolonging gestation in the rabbit. Its tocolytic effects may be mediated, in part, by alterations in cervical MMP activity.

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A dose-dependent beneficial effect was observed on leakage of evans blue dye in skin challenged with antigen and on paw anaphylaxis induced by antiserum. The compound 1 also exhibited significant (P<0.01) inhibition of rat paw edema and granuloma tissue formation, including significant protection of RBC against the haemolytic effect of hypotonic solution, an indication of membrane-stabilizing activity.

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1-Methylnicotinamide (MNA) is a primary metabolite of nicotinamide recently proven to cause systemic increase in PGI(2) plasma levels in an unknown mechanism. Our present study was aimed at verifying whether the increased production of PGI(2), a vasodilating prostanoid, in response to MNA, its metabolite N-methyl-2-pyridone-5-carboxamide (Met2PY), and nicotinamide may be reproduced under in vitro conditions. Since prostacyclin is a vasodilating prostanoid, we also performed the functional tests in the ex vivo model of coronary vascular bed perfusion to evaluate the vasoactive properties of those compounds. We did not observe any significant effect of the tested drugs on either PGI(2) or PGE(2) secretion in our in vitro model. Nicotinamide at the concentrations of 10 and 100 μmol/l and 100 μmol/l Met2PY slightly but significantly increased coronary flow in rat heart. These increases, however, remained very low when compared to that induced by the reference compound, bradykinin (100 nmol/l). Perfusion of rat hearts with Met2PY in the presence of 50 μmol/l indomethacin resulted in decreased coronary flow, which proves that the effect is cyclooxygenase dependent. We conclude that MNA metabolites should be more carefully addressed in reference to pro-prostacyclin activity and that systemic mechanism of MNA-induced PGI(2) production needs further clarification.

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Studies were identified by searching electronic databases and writing to manufacturers. We selected randomised double blind trials comparing topical NSAID with either placebo or another active treatment in adults with acute pain, and extracted dichotomous information approximating to a 50% reduction in pain at one week, together with details of adverse events and withdrawals. Relative benefit and number-needed-to-treat (NNT), and relative risk and number-needed-to-harm (NNH) were calculated, with sensitivity analyses where appropriate to investigate differences between individual drugs and aspects of trial design.

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Plectranthus amboinicus (P. amboinicus) is a folk herb that is used to treat inflammatory diseases or swelling symptoms in Taiwan. We investigated therapeutic efficacy of P. amboinicus in treating Rheumatoid Arthritis (RA) using collagen-induced arthritis animal model. Arthritis was induced in Lewis rats by immunization with bovine type II collagen. Serum anti-collagen IgG, IgM and C-reactive protein (CRP) were analyzed. To understand the inflammation condition of treated animals, production of TNF-α, IL-6 and IL-1β from peritoneal exudates cells (PEC) were also analyzed. P. amboinicus significantly inhibited the footpad swelling and arthritic symptoms in collagen-induced arthritic rats, while the serum anti-collagen IgM and CRP levels were consistently decreased. The production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β were also decreased in the high dosage of P. amboinicus group. Here, we demonstrate the potential anti-arthritic effect of P. amboinicus for treating RA, which might confer its anti-rheumatic activity. This differs the pharmacological action mode of indomethacin.

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Maximum ulceration, observed on the 3rd day after indomethacin administration was effectively healed by mal B and mal C (each 10 mg/kg, p. o. x 3 days), the latter showing equivalent potency (~78% p < 0.001) as that of Omez (3 mg/kg, p. o. x 3 days) and misoprostol (10 mug/kg, p. o. x 3 days). Compared to the untreated mice, those treated with mal B or mal C respectively for 3 days increased the mucosal EGF level (139 and 178%, p < 0.001), the serum VEGF level (56%, p < 0.01 and 95%, p < 0.001) and microvessels formation (37%, p < 0.05 and 62%, p < 0.01), while reducing the serum endostatin level (37%, p < 0.05 and 61%, p < 0.01). The relative healing capacities of mal B and mal C correlated well with their respective abilities to modulate the angiogenic factors. The healing by Omez and misoprostol was not due to improved angiogenesis.

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The chemical advances of the 20th century led to the synthesis of non steroidal anti-inflammatory drugs (NSAIDs), beginning from phenylbutazone and indomethacin and continuing with other new drugs, including ibuprofen, diclofenac, naproxen, piroxicam and, more recently, the highly selective COX-2 inhibitors (coxibs). This progress derived from the discovery of the mechanism of action Cordarone Online of these drugs: the inhibition of synthesis of prostaglandins due to the cycloxigenase enzyme system, according to the experimental contributions of John R. Vane.

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Prostaglandin E(2) (PGE(2)) plays a major role both in maintaining patency of Zithromax Online Uk the fetal ductus arteriosus and in closure of the ductus arteriosus after birth. The rate-limiting step in PGE(2) signal termination is PGE(2) uptake by the transporter PGT.

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A gastroprotective effect occurs when α(2) receptors are innervated. The dextro isomer of medetomidine, dexmedetomidine, is a highly selective α(2)-adrenoreceptor agonist. The aim of this study was to investigate whether dexmedetomidine has an antiulcerative effect and to show whether the antiulcer mechanism of dexmedetomidine is linked with oxidant/antioxidant parameters. The antiulcerative effect of dexmedetomidine was studied in an indomethacin-induced ulcer model, and some oxidant/antioxidant parameters were measured in these gastric tissues. Whereas the average ulcerous areas for the groups that received 10, 25, 50, and 100 μg/kg dexmedetomidine doses were 29 ± 4.2, 8 ± 2.1, 0 ± 0 and 0 ± 0 mm(2), respectively, the ulcerous area was 52.1 ± 4.5 mm(2) in the indomethacin control group and 0.5 ± 0.2 mm(2) in the famotidine group. In conclusion, the α(2)-adrenoreceptor agonist dexmedetomidine showed a significant antiulcerative effect in rat gastric tissue at all doses. This antiulcerative effect is stronger with increasing dosage; at the 50 Cymbalta Generic Patent and 100 μg/kg doses, no ulcerous areas were observed. In light of these results, we conclude that there is a correlation between antiulcer mechanisms and α(2)-receptor activation. In rats given dexmedetomidine, all of the investigated antioxidant parameters increased, except for catalase (CAT). Conversely, aside from myeloperoxidase (MPO), all oxidant parameters decreased. Therefore, oxidant/antioxidant parameters play a role in the antiulcer mechanism of dexmedetomidine.

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Supercritical carbon dioxide (sc-CO(2)) was used to impregnate indomethacin (a non-steroidal anti-inflammatory drug) into chitosan thermosets for the preparation of controlled release formulations. The products were analyzed by a range of methods including powder X-ray diffraction (XRD) and scanning electron microscopy (SEM). The effects of the experimental temperature and pressure of the sc-CO(2) on the thermal behavior of chitosan-indomethacin drug composites (DCs) was investigated via differential scanning calorimeter ( Cialis Generic Forum DSC). The interaction of chitosan and indomethacin after impregnation was then studied by Fourier transform infrared (FTIR) and Raman spectroscopy, respectively. Our results suggest that the supercritical fluid impregnation process results in indomethacin being amorphously dispersed within the chitosan matrix. FTIR data suggest that the aliphatic carbonyl group of indomethacin interacts with the NH(2) group of the chitosan backbone. In vitro dissolution studies (via UV-vis spectroscopy) reveal that the dissolution rate of indomethacin substantially increases after processing in sc-CO(2), particularly, under the experimental conditions 20.7 MPa and 70 degrees C.

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Glibenclamide' Motilium Generic s effects on agonist-induced constrictions are unlikely to be via an inhibition of ATP-sensitive K+ channels, and with U46619- and U44069-induced constrictions, glibenclamide may be acting as a competitive antagonist of thromboxane receptors.

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Triphala has a promising anti-inflammatory effect in Oxytrol Generic the inflamed paw of arthritis-induced rats.

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Physicochemical properties of the new synthesized compound confirmed the formation of IFM. Incubation of IFM in the contents of the GI tract and plasma revealed that IFM was not relatively stable in GI contents during the time period of transit through the GI tract, whereas it was very unstable in plasma and released 5FU rapidly. The IFM dry emulsion could be easily reconstituted in water, and the mean particle size was 2.416 microm. The absorption rate constant (K) for IFM with concentration of 2, 5, and 10 microg/mL in Cost Cytoxan Iv the in situ perfusion experiment were 0.473, 0.423, and 0.433/h, respectively, demonstrating passive diffusion of IFM across the biological membranes.

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The aim of the current study was to investigate the vasorelaxant activity of five structurally-related triterpenic acids namely ursolic (1), moronic (2), morolic (3), betulinic (4) and 3,4-seco-olean-18-ene-3,28-dioic (5) acids. The vasorelaxant effect of compounds 1-5 were determined on Lipitor Generic Price endothelium-denuded and endothelium-intact rat aortic rings pre-contracted with noradrenaline (0.1 μM). All compounds showed significant relaxant effect on endothelium-intact vessels in a concentration-dependent manner (p<0.05). Ursolic, moronic and betulinic acids were the most potent vasorelaxant agents with 11.7, 16.11 and 58.46 μM, respectively. Since vasorelaxation was blocked by L-NAME, while indomethacin did not inhibit the effect, endothelium-derived nitric oxide seems to be involved in triterpenic 2 and 3 mode of action. Compounds 1-5 were docked with a crystal structure of eNOS. Triterpenes 1-5 showed calculated affinity with eNOS in the C1 and C2 binding pockets, near the catalytic site; Ser248 and Asp480 are the residues that make hydrogen bonds with the triterpene compounds.

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In euvolaemic preterm neonates with HPS and the need for excessive replacement of salt and water, inhibition of renal PGE(2) excretion with indomethacin effectively reduces polyuria and natriuresis without acutely compromising Cefixime Cost Philippines renal function.

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MRP2 is an efflux transporter that is expressed mainly in the canalicular membrane of hepatocytes, where it expels polar and ionic compounds into the bile. MRP2 is also present in the apical membrane of enterocytes and epithelial cells of proximal tubules of the kidney. Inhibition of MRP2 transport can lead to the accumulation of metabolites and other MRP2 substrates up to toxic levels in these cells. The transport properties of MRP2 are frequently studied with the vesicular transport assay. The assay identifies compounds that interact with MRP2 by measuring the effect of a compound on the transport of a radioactively labeled or fluorescent probe. We have compared the effect of eight selected test compounds (quercetin, disopyramide, paracetamol, indomethacin, diclofenac, estrone-3-sulfate, budesonide, and thioridazine) on the MRP2-mediated transport of three commonly used probes: 5(6)-carboxy-2,7-dichlorofluorescein, leukotriene C4 and estradiol-17-β-d Bystolic Generic Equivalent -glucuronide (E217βG). Five of the test compounds had different probe-dependent effects on the MRP2-mediated transport, suggesting differences in the transport mechanism of the probes. Our results underline the complexity of substrate recognition by these efflux transporters and the difficulties in directly comparing results obtained with different assays, especially when different probes are used.