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Celebrex (Celecoxib)

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Generic Celebrex is a high-powered medication in battle against arthritis (rheumatoid arthritis, osteoarthritis), ankylosing spondylitis and painful menstruation. Generic Celebrex can be helpful for patients with problems of stomach, intestines, heart, circulation, and FAP (familial adenomatous polyposis). Generic Celebrex acts as popular medicine which can not only provide treatment of arthritis but also it protects from painful menstruation.

Other names for this medication:

Similar Products:
Motrin, Naprosyn, Anaprox, Mobic, Indocin


Also known as:  Celecoxib.


Generic Celebrex is produced with efficacious pharmacy formula making Generic Celebrex wonderful weapon against arthritis (rheumatoid arthritis, osteoarthritis), painful menstruation, inflammation, fever, joint pain, swelling and tenderness. Target of Generic Celebrex is to prevent pain and inflammation.

Generic Celebrex acts as popular medicine which can not only provide treatment of arthritis but also it protects from painful menstruation. Generic Celebrex acts blocking hormones of pain and inflammation.

Celebrex is also known as Celecoxib, Celebra, Cobix, Celcoxx, Selecap.

Generic Celebrex is NSAID (anti-inflammatory drug).

Generic name of Generic Celebrex is Celecoxib.

Brand names of Generic Celebrex are Celebrex, Celebra.


Generic Celebrex is available in capsules which should be taken by mouth meal or milk.

It is better to take Generic Celebrex every day.

Take Generic Celebrex and remember that its dosage depends on patient's health state.

For treatment of rheumatoid arthritis

Usual Generic Celebrex dosage is 100-200 mg twice a day.

For treatment of osteoarthritis

Usual Generic Celebrex dosage is 100 mg twice a day or 200 mg once a day.

For treatment of painful menstruation

Usual Generic Celebrex dosage is 400 mg once a day at the first day of treatment. In case you need, the dosage of 400 mg can be divided into double dose and can be taken twice a day.

For treatment of FAP

Usual Generic Celebrex dosage 400 mg twice a day.

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


If you overdose Generic Celebrex and you don't feel good you should visit your doctor or health care provider immediately.


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 Celebrex 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.


Do not take Generic Celebrex if you are allergic to Generic Celebrex components or to aspirin.

Do not take Generic Celebrex if you are pregnant, planning to become pregnant. It is unknown if Generic Celebrex is excreted in breast milk. Avoid breast-feeding.

Generic Celebrex can't be given to children under 2 years.

Generic Celebrex can't be given to patients who experience bypass surgery.

Do not use allergy and pain medicines at the same time with Generic Celebrex.

Try to be careful with Generic Celebrex in case of using such medications as (Mavik), quinapril (Accupril), ACE inhibitor (captopril (Capoten), benazepril (Lotensin), lisinopril (Zestril, Prinivil), ramipril (Altace), enalapril (Vasotec), fosinopril (Monopril), moexipril (Univasc), perindopril (Aceon), blood thinner as warfarin (Coumadin), aspirin or other NSAIDs (mefenamic acid (Ponstel), etodolac (Lodine), diclofenac (Voltaren), ibuprofen (Advil, Motrin), piroxicam (Feldene),naproxen (Aleve, Naprosyn), flurbiprofen (Ansaid), ketorolac (Toradol), ketoprofen (Orudis), nabumetone (Relafen), meloxicam (Mobic)), methotrexate (Rheumatrex, Trexall), diuretics (furosemide (Lasix)), lithium (Eskalith, Lithobid).

Be careful with Generic Celebrex in case of having liver, heart or kidney disease, asthma, high blood pressure, stroke, stomach ulcers, bleeding or blood clotting disorder, congestive heart failure, epilepsy.

Be careful with sunbeams. Generic Celebrex makes skin sensitive to sunlight. Protect skin from the sun.

Avoid alcohol.

It can be dangerous to stop Generic Celebrex taking suddenly.

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To investigate the relationship between acute coronary syndrome (ACS) and ingested doses of selective cyclooxygenase-2 (COX-2) inhibitors and other nonsteroidal anti-inflammatory drugs (NSAIDs).

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There were no differences between the non-steroid and steroid groups with regard to VAS at rest and during activity, or range of motion, at any postoperative observation time. The postoperative Knee Society Knee Score in the steroid group improved significantly as compared with that in non-steroid group at the one-month (84.1±13.1 and 65.9±12.1; P < 0.0045), three-month follow-up (90.2±16.3 and 72.5±16.6; P < 0.0027), but after postoperative six-month the Knee Society Knee Score showed no significant difference between the groups. There was no significant difference in consumption of the morphine about daily or total consumption within 72 hours between the two groups. The duration of celecoxib usage in patients in the steroid group was significantly shorter than that in the non-steroid group ((7.2±0.7) compared with (10.5±1.9) weeks; P = 0.012).

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Use of NSAIDs is associated with an increased risk of HF exacerbation among patients with pre-existing HF. The excess risk was approximately 40% for conventional NSAIDs and celecoxib. The highest risk was observed among rofecoxib users.

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Oxaliplatin (OXA) is the common and extremely potent anti-advanced colorectal cancer chemotherapeutic. Accumulating evidence reveals that OXA evokes mechanical and cold hypersensitivity. However, the mechanism underlying these bothersome and dose-limiting adverse effects is poorly understood. It is well known that cyclooxygenase-2 (COX-2) as well as phosphoinositide 3-kinase (PI3K)/Akt signaling mediate the neuropathic pain. But it is still unclear whether COX-2 or PI3K/Akt signaling participates in the regulation of OXA-induced hypersensitivity, as well as the linkage between COX-2 and PI3K/Akt signaling in mediating OXA-induced hypersensitivity. In this paper, we investigated the anti-nociceptive effect of celecoxib, an inhibitor of COX-2, on the OXA-induced neuropathic pain. We found that OXA increased the expression of cyclooxygenase-2 (COX-2) and Akt2 in the lumbar 4-5 (L4-5) dorsal root ganglion (DRG). And the administration of celecoxib alleviates the OXA-induced hypersensitivity and suppresses the COX-2 and PI3K/Akt2 signaling. Our findings showed that COX-2 and PI3K/Akt2 signaling in DRG contributed to the OXA-induced neuropathic pain. In addition, celecoxib enhanced the OXA-induced mortality of the human colon cancer cell line HCT-116. Thus, celecoxib might play a dual role in colorectal cancer treatment: alleviating OXA-induced neuropathic pain and facilitating the anti-tumor effects of OXA through their synergistic role.

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The expression of COX-2, IL-1alpha, IL-6, IL-8, IL-11, and TNF-alpha, as well as PGE(2) production increased in the presence of IL-17A, whereas COX-1 expression did not change. Celecoxib blocked the stimulatory effect of IL-17A on the expression of COX-2, IL-1alpha, IL-6, IL-8, and IL-11 as well as PGE(2) production, whereas it did not block TNF-alpha expression. Cycloheximide pretreatment suppressed the expression of IL-17-induced inflammatory cytokines. The expression of IL-1alpha, IL-6, IL-8, and IL-11 increased by the addition of PGE(2), whereas TNF-alpha expression was not affected.

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Since 1998, two selective inhibitors of COX-2 have been approved in many countries for the treatment of rheumatoid arthritis, osteoarthritis and acute pain. These new drugs have a significantly reduced gastrointestinal toxicity when compared with non-selective COX inhibitors. However, the results of two large clinical trials conducted in patients with osteoarthritis and rheumatoid arthritis have recently raised some concerns regarding the cardiovascular safety of these new drugs. The purpose of this paper is to review the potential mechanisms whereby selective COX-2 inhibitors could increase the cardiovascular risk of patients and to analyse the data indicating that this clinical risk indeed exists. The authors' analysis shows that even though there are pathophysiological mechanisms which could explain why selective COX-2 inhibition might increase the cardiovascular risk in patients, the actual level of evidence demonstrating that the risk is indeed increased is weak. Because of the importance of the issue, additional studies must be conducted with this class of agents. Meanwhile, it is crucial to emphasise that neither selective COX-2 inhibitors nor conventional NSAIDs replace aspirin in patients with a high cardiovascular risk.

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The restricted group had significantly less use of celecoxib, indicating that restriction was effective at reducing celecoxib utilization. Although limitations exist when comparing populations from different health plans, and the underlying causes of serious GI complications are multifactorial, the restricted group had a higher incidence of serious GI complications and higher costs related to serious GI complications and arthritis.

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This meta-analysis supports an increased risk of ischemic stroke with the current use of rofecoxib and diclofenac. Additional studies are required to evaluate most individual NSAIDS, the effect of dose and duration, and the subtypes of stroke.

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Novel tricyclics were synthesized and evaluated in vitro for their COX-1/COX-2 inhibitory activities and their abilities to inhibit cell proliferation in prostate (AT3B-1, PC-3 and LNCaP) and breast (MCF-7) cancer cell lines. A molecular modeling study was carried out to characterize the electronic nature of the central ring systems of the novel tricyclic COX-2 inhibitors.

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The results of this literature review showed an unclear role in CRC prevention of both pharmacological and dietary intervention. Despite several options are available to prevent colon cancer, it is challenging to identify a correct strategy to prevent CRC through pharmacological and dietary intervention due to the long latency of cancer promotion and development. Since some of the drugs investigated may have uncertain individual effects, it can be suggested to potentiate such effects by adding them together.

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The successful pain relief of the patient in this case indicates that treatment of pain that based on mechanism might be worth promoting. According to the etiology of pain, specific drugs or measures should be selected for the individual patient. This approach have certain advantages, such as timely pain relief, reduction of medical cost, and effective improvement of life quality of cancer patients.

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Messenger RNA (mRNA) and protein expression were analyzed by Northern and Western analysis, respectively, to determine the level of enzymes induced by Ras. In vitro assays were used to determine the production of vascular endothelial growth factor (VEGF) and prostaglandins as well as the promoter and enzymatic activation of the rate-limiting enzyme in prostaglandin production (phospholipase A(2) [cPLA(2)]).

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Traumatic heterotopic ossification (HO) is a common clinical condition associated with various orthopedic procedures that involve injury to soft tissues near bone. In this study, we tested the hypothesis that the prophylactic effects of NSAID's in the treatment of HO are mediated via inhibition of the COX-2 enzyme. Here we describe a rat model that simulates HO in the human that was used to test the above hypothesis.

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Familial adenomatous polyposis (FAP) is a rare genetic disease. Without treatment, FAP patients have a 100% lifetime risk of developing colorectal cancer. This study was conducted to evaluate the effect of celecoxib treatment in prolonging the time to FAP-related events and to document the safety profile of the long-term use of celecoxib (≥6 months) in FAP patients. FAP patients receiving celecoxib in routine clinical practice were individually matched with historical/concurrent FAP patients not receiving celecoxib. The study population included patients aged 12 years or older registered in national and regional FAP registries in Denmark, the United States, Spain, and Canada. Descriptive statistics were used to summarize dose and duration among celecoxib treated patients. The primary study endpoints, time-to-next-FAP events, were examined with Kaplan-Meier method. Fifty four celecoxib-treated patients were recruited and a matched control was identified for 13 of these patients. The Kaplan-Meier estimated probability of not having a polypectomy 12 and 60 months post- ileorectal anastomosis in the celecoxib-treated patients (n = 33) was 60.6% and 42.2%, respectively. The estimated probability of not having a polypectomy 6-60 months post-ileal pouch-anal anastomosis the celecoxib-treated patients (n = 24) was 100%. The median total daily dose of celecoxib was 698.9 mg with the majority treated more than 24 months. Five celecoxib-treated patients experienced 6 serious adverse events with one of these events (rash) considered related to celecoxib. Long term celecoxib treatment appeared to be well tolerated in FAP patients with or without FAP-related surgeries.

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A new and simple high-performance liquid chromatography assay was developed and validated for the simultaneous determination of the above-mentioned drugs in small samples of human plasma (0.25 mL). After protein precipitation with acetonitrile, satisfactory separation was achieved on a Hypersil BDS C18 column (250 × 4.6 mm, 5 m) using a mobile phase comprising 20 mmol/L ammonium phosphate buffer (pH = 3) and acetonitrile at a ratio of 35:65, vol/vol; the elution was isocratic at ambient temperature with a flow rate of 1 mL/min. The UV detector was set at 265 nm.

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Celecoxib seems safer than rofecoxib and NSAIDs in elderly patients with congestive heart failure. Differences were found among cyclo-oxygenase-2 inhibitors.

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Obsessive-compulsive disorder is a common neuropsychiatric condition. Although a variety of pharmaceutical agents is available for its treatment, psychiatrists have found that many patients cannot tolerate the side effects, do not respond to treatment adequately, and may finally discontinue their treatment. However, augmentation strategies have been shown to have some benefits in the treatment of OCD. These include reducing both the overall cost of treatment and the side effects. The purpose of this study was to assess the efficacy of celecoxib as an adjuvant agent in the treatment of OCD in an 8-week, double-blind, placebo controlled trial. To this end, 25 patients were assigned to a study group and were given fluoxetine 20mg/day plus celecoxib 400mg/day (200mg BID). The control group included 25 patients who were given fluoxetine 20mg/day plus placebo. Both protocols significantly lowered scores on the Yale-Brown Obsessive-Compulsive Scale over the trial period. The combination of fluoxetine and celecoxib decreased the symptoms of obsessions and compulsions significantly more than fluoxetine plus placebo. The results of this study suggest that celecoxib can be an effective adjuvant agent in the management of patients with OCD; therefore, anti-inflammatory therapies should be further investigated.

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This investigation demonstrated a functional coupling between cyclooxygenase-1 (cox) and prostaglandin E2/D2 biosynthesis in murine skin repair. Cyclooxygenase-1 expression decreased transiently after excisional wounding, and this was followed by a marked fall in the rate of prostaglandin E2/D2 biosynthesis at the wound site. Expression of cyclooxygenase-1, prostaglandin synthases, and prostaglandin E2/D2 production were colocalized in new tissue at the margin of the wound. Although cyclooxygenase-2 expression was strongly induced in granulation tissue on injury, this isoform did not contribute to high prostaglandin E2/D2 concentrations in wounds. Accordingly, wound tissue from SC-560-treated mice (selective cyclooxygenase-1 inhibitor) and diclofenac-treated mice (nonselective cyclooxygenase inhibitor), but not celecoxib-treated mice (selective cyclooxygenase-2 inhibitor), and wound tissue from cyclooxygenase-1-deficient animals exhibited a severe loss of prostaglandin E2/D2 at the wound site, and this change was associated with an impairment in the normal wound morphology. Topically administered prostaglandin E2 (dinoprostone) was able to restore normal wound repair to diclofenac-treated mice. In contrast to the presence of an injury-induced cyclooxygenase-2, these data constitute strong evidence that cyclooxygenase-1-coupled prostaglandin E2/D2 biosynthesis has a central role in skin repair.

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The novel cyclooxygenase- (COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis and rheumatoid arthritis. Conventional treatment for these debilitating conditions routinely involves the use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs), which are nonspecific inhibitors of COX-1 and COX-2. Numerous studies suggest that inhibition of renal prostaglandin synthesis by NSAIDs is deleterious to kidney function, particularly in high-risk patients. As celecoxib inhibits COX-2 and spares COX-1 at therapeutic doses, we hypothesized that it may offer an improved renal safety profile in patients at risk for NSAID-induced renal toxicity. This article represents a post hoc analysis of the renal safety of celecoxib, using the safety database generated during its clinical development program. This analysis includes data from more than 50 clinical studies involving more than 13,000 subjects. Most subjects were enrolled in randomized, controlled trials (of up to 12 weeks' duration); however, more than 5000 subjects received celecoxib for as long as 2 years in a long-term, open-label study at as much as twice the maximum recommended dosage. The overall incidence of renal adverse events after celecoxib was greater than that after placebo but similar to that after NSAIDs. The most common events reported after celecoxib, namely, peripheral edema (2.1%), hypertension (0.8%), and exacerbation of preexisting hypertension (0.6%), were not time- or dose-related. Peripheral edema was not associated with increased weight or blood pressure. Furthermore, there was no evidence of drug-drug interactions between celecoxib and concomitant angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics. We conclude that celecoxib is well tolerated by patients who may be at risk for NSAID-induced renal toxicity, such as the elderly and those with hypertension or preexisting chronic heart disease.

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From relevant reports, 114 randomized double-blind clinical trials were included.

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HPV16(+/-) mice presented higher CD8(+) T cell infiltration than HPV16(-/-) animals (P<0.001). Older HPV16(+/-) animals showed epidermal dysplasia and increased percentages of CD8(+)CD107a(+) T cells compared with younger animals with hyperplasia (P<0.001), validating this model for testing the effects of celecoxib on CD8(+) T cells. CXB-treated HPV16(+/-) mice showed higher percentages of CD8(+)CD107a(+) T cells compared with untreated HPV16(+/-) animals (P<0.01), but no differences were observed concerning the progression of epidermal lesions.

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buy celebrex usa 2017-04-29

Low pretreatment plasma levels of VEGF appear celebrex buy to be predictive of a positive effect of celecoxib on survival.

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To investigate the role celebrex buy of cyclooxygenase (COX) isozymes (COX-1 and -2) in the regulation of bladder volume capacity (BVC) in several rat urodynamic models, using a selection of nonsteroidal anti-inflammatory drugs (NSAIDs), some selective for COX-2, correlating the potency of the tested compounds in the urodynamic models and their in vitro potency as inhibitors of COX isozymes, to verify the relative importance of the different isozymes.

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New series of 3,4-diaryl-2-thioxoimidazolidin-4-ones and 3-alkylthio-4,5-diaryl-4H-1,2,4-triazoles were designed, synthesized and evaluated for their activity as anti-inflammatory agents. Compounds 20, 21, 23 and 34 are highly selective inhibitors of COX-2 enzyme at a concentration of 100 mM Prograf Dose Adjustment relative to celecoxib, the standard reference. (±)-3-(4-Phenoxy-phenyl)-5-phenyl-2-thioxoimidazolidin-4-ones 23 exhibited the most active anti-inflammatory agent.

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Isomeric iodinated derivatives of nimesulide, with an iodine substituent on the phenoxy ring, were prepared with the aim of identifying potential candidate compounds for the development of imaging agents targeting cyclooxygenase-2 (COX-2) in the brain. Both the experimental logP7.4 and pKa values for these iodinated analogs were in the acceptable range for passive brain penetration. The para-iodo-substituted analog was a more potent and selective COX-2 inhibitor than nimesulide, with Symmetrel 200 Mg a potency that was comparable to the reference drug, celecoxib. Iodination at the ortho- or meta-position of the phenoxy ring was associated with a substantial loss of COX-2 inhibitory activity. Transport studies across Caco-2 cell monolayers in the presence and absence of a P-glycoprotein (P-gp) inhibitor, verapamil, indicated that the para-iodo-substituted analog was not a P-gp transport substrate; this feature is a prerequisite for potential in vivo brain imaging compounds. The para-iodo-substituted analog of nimesulide appears to be an attractive candidate for the development of radioiodine-labeled tracers for in vivo brain imaging of COX-2 levels.

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Nonsteroidal anti-inflammatory drugs are among the most widely prescribed medications. Their effect on blood pressure has been monitored, and many small studies have determined a potential relationship between their use and elevation of blood pressure. These drugs may affect blood pressure by inhibiting prostaglandin synthesis, which may affect arteriolar smooth muscle tone and natriuresis. Since many patients with conditions such as osteoarthritis require treatment and also have hypertension, even modest elevations in blood pressure or inhibition of antihypertensive medication efficacy resulting from non steroidal anti-inflammatory drugs can be of significant clinical and public health importance. This review finds that certain drugs (e.g., indomethicin, piroxicam, and naproxen) may cause clinically relevant Levitra Dosage Recommendations elevations in blood pressure in hypertensive patients. Aspirin and sulindac do not appear to elevate blood pressure significantly, even in hypertensive patients. Ibuprofen and other nonsteroidal anti-inflammatory drugs appear to have an intermediate blood pressure effect. Cyclo-oxygenase-2 inhibitors such as refecoxib and celecoxib have been shown to cause mild elevations in blood pressure, but further studies are needed to evaluate the full magnitude and population distribution of this effect. (c)2000 by Le Jacq Communications, Inc.

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The ocular pharmacokinetics of SAR 1118 were studied in rats after a single topical dose of (14)C-SAR 1118 (1 mg/eye; 40 μCi; 15.5 μL). SAR 1118 concentration time profiles in plasma and ocular tissues were quantified by liquid scintillation counting (LSC). The pharmacologic activity of SAR 1118 eye Glucotrol Gel drops administered thrice daily for 2 months at 1% (0.3 mg/eye/d) and 5% (1.5 mg/eye/d) was assessed in an STZ-induced diabetic rat model by determining retinal leukostasis and blood-retinal barrier breakdown. Diabetic rats treated with periocularly administered celecoxib microparticles served as the positive control, and vehicle-treated rats served as the negative control.

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This study demonstrated, for the first time in a 2-year randomised controlled trial using qMRI, the Accutane Generic Cost superiority of CS over celecoxib at reducing CVL in knee OA patients.

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Breast reduction has traditionally been performed under general anesthesia with adjunct opioid use. However, opioids Legal Online Cialis are associated with a wide variety of adverse effects, including nausea, vomiting, constipation, postoperative sedation, dizziness, and addiction.

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1. The maintenance of renal function in decompensated cirrhosis is highly dependent on prostaglandins (PGs). Since PG synthesis is mediated by cyclooxygenase-1 and -2 (COX-1 and COX-2), the present study was designed to examine which COX isoform is involved in this phenomenon. 2. Renal COX-1 and COX-2 protein expression and distribution were analysed by Western blot and immunohistochemistry in nine rats with carbon tetrachloride-induced cirrhosis and ascites and 10 control animals. The effects of placebo and selective COX-1 (SC-560) and COX-2 (celecoxib Motilium 40 Mg ) inhibitors on urine flow (V), urinary excretion of sodium (U(Na)V) and PGE(2) (U(PGE2)V), glomerular filtration rate (GFR), renal plasma flow (RPF), the diuretic and natriuretic responses to furosemide and renal water metabolism were assessed in 88 rats with cirrhosis and ascites. 3. COX-1 protein levels were found to be unchanged in kidneys from cirrhotic rats. In contrast, these animals showed enhanced renal COX-2 protein expression which was focally increased in the corticomedullary region. Although U(PGE2)V was equally reduced by SC-560 and celecoxib, only SC-560 produced a significant decrease in U(Na)V, GFR and RPF and a pronounced impairment in the diuretic and natriuretic responses to furosemide in rats with cirrhosis and ascites. Neither SC-560 nor celecoxib affected renal water metabolism in cirrhotic rats. 4. These results indicate that despite abundant renal COX-2 protein expression, the maintenance of renal function in cirrhotic rats is mainly dependent on COX-1-derived prostaglandins.

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The effects of Celecoxib on the proliferation of PC-3 cells were observed by MTT assay, erosion trace test and Transwell-chamber chemotaxis assay, and their apoptosis detected by Annexin Suprax Medication Coupons V/FITC fluorescent staining and flow cytometry.

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Increased level of cyclooxygenase-2 (COX-2) plays a significant role in the pathogenesis of cancers. High expression of COX-2 has been demonstrated in several cancer types including retinoblastoma. However, the in vivo study did not confirm the anti-proliferative effect of COX-2 inhibitor, celecoxib, on a murine transgenic retinoblastoma model. We, therefore, aim to investigate COX-2 expression in paraffin-embedded retinoblastoma specimens in a larger study group.

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Information on publication year, participant characteristics, trial duration, drug, control, dose, and events were extracted using a standardized protocol.

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To systematically review the literature on the safety of using nonsteroidal antiinflammatory drugs (NSAID) and/or paracetamol in people receiving methotrexate (MTX) for inflammatory arthritis (IA), as an evidence base for generating clinical practice recommendations.

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PGE(2) can be measured in NAF. PGE(2) levels are concentrated in NAF when compared with matched plasma samples. Celecoxib 200 mg b.i.d. does not appear to significantly decrease PGE(2) concentrations in NAF and plasma.

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Both COX-2 selective inhibitors (coxibs) and nonselective (ns)-NSAIDs elevate blood pressure (BP) and this may contribute to excess cardiovascular (CV) events. A number of recent large-scale randomized clinical trials (RCTs) comparing coxibs (including newer agents, lumiracoxib and etoricoxib) to both ns-NSAIDs and placebo have been reported, permitting an update to earlier BP analyses of these agents.

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To establish the efficacy and safety of rofecoxib in the management of OA by systematic review of available evidence.

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Extensive use of rofecoxib, celecoxib, and diclofenac increases the risk of acute myocardial infarction, but similar use of ibuprofen and naproxen does not.

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Familial Adenomatous Polyposis (FAP) is an autosomal dominant disorder characterized by colonic polyps in early adult life. Children with this disease are at risk for colonic cancer, so prophylactic colectomy is the standard treatment to prevent this complication. Chemoprevention experience with NSAIDs in children is exceptional. This case report describes our experience with Celecoxib, a COX-2 inhibitor, in a 12-year-old boy.

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Celecoxib is as effective as other nonsteroidal anti-inflammatory drugs (NSAIDs) for treating the symptoms of osteoarthritis or rheumatoid arthritis. However, patients taking celecoxib are less likely to discontinue the medication because of gastrointestinal upset than patients taking traditional NSAIDs. Nevertheless, celecoxib does not decrease the incidence of serious gastrointestinal adverse events with long-term therapy.

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The experimental model was considered to be successful because 78% of the rats in the control group developed liver tumors. The number of neoplastic lesions was similar among the celecoxib, indomethacin and control groups, although the nodule diameter of the lesions was smaller in the celecoxib group. Better results were observed in animals that received celecoxib at doses of 6 and 9 mg/kg/ day; 4 rats in these groups did not show any neoplastic histological lesions, and a greater proportion of the nodules in the other animals in these groups were benign than in the groups that did not use celecoxib.

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To evaluate the pharmacokinetic and pharmacodynamic (anti-arthritic) herb-drug interactions of A. paniculata Nees extract (APE) and pure andrographolide (AN) with etoricoxib (ETO) after oral co-administration in wistar rats.

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The level of scar elevation decreased in the captopril group and the level of infiltration of inflammatory cells decreased in the celecoxib group. In the group where a combination of the 2 drugs was used, the level of scar elevation decreased the most, and collagen deposition and organization returned to normal most rapidly. Celecoxib was found to inhibit the initial inflammation in the ear wound of the rabbit, and captopril inhibited scar elevation.

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We found that large numbers of infiltrating MDSC co-localise with COX-2 expression in those areas where tumour growth takes place. Celecoxib reduced prostaglandin E2 levels in vitro and in vivo. Treatment of tumour-bearing mice with dietary celecoxib prevented the local and systemic expansion of all MDSC subtypes. The function of MDSC was impaired as was noticed by reduced levels of ROS and NO and reversal of T cell tolerance; resulting in refinement of immunotherapy.

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Our results confirm the usefulness of docetaxel for HRPC treatment and show a significant reduction of haematological toxicity with bi-weekly docetaxel administration combined with celecoxib.

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After macrophages were stimulated with lipopolysaccharide (LPS)+interferon-gamma (IFN-gamma) in the presence or absence of celecoxib for 24 h, the cell-free supernatant of LPS-stimulated macrophages was transferred to the culture of NSC34 cells. Viability of NSC34 cells was assessed by MTT assay after a further 24 h and 72 h incubation. After macrophages were stimulated by LPS+IFN-gamma for 12 h or 24 h, the release of prostaglandin E2 (PGE2), nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) from macrophages was measured by radioimmunoassay, Griess assay, fluorescence assay and enzyme-linked immunosorbent assay, respectively. The mRNA levels of COX-2, inducible nitric oxide synthase (iNOS), TNF-alpha and IL-1beta in macrophages were determined by reverse transcription-polymerase chain reaction after macrophages were stimulated for 6 h and 12 h.

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To assess the analgesic efficacy and adverse effects of a single oral dose of celecoxib for moderate to severe postoperative pain.

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The structured regime consisting of total intravenous anaesthesia (propofol-remifentanil), well defined fluid administration, prophylactic antiemetics (dexamethasone, ondansetron, droperidol), weak analgesics (celecoxib, paracetamol) and intraoperative epidural analgesia (bupivacaine, morphine) was feasible in more than 90% of all patients. In the postanaesthesia care unit, 64% did not require opioids, but 25% experienced severe pain. Mean length of stay was 2 h with a mean discharge readiness of 80 min. Half the patients required supplemental oxygen for 1 h or more to sustain an SpO2 greater than 92%, and 8% experienced nausea or vomiting. A complicated recovery, defined as the presence of severe complaints (pain, nausea or vomiting), with more than five treatment interventions in the postanaesthesia care unit, or a length of stay more than 2 h, was seen in 52%.

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It was found that EPC could elicit potent cardioprotection against I-R injury, shown by reduction of infarct size and improvement of ultrastructural organisation; whereas administration of celecoxib resulted in complete loss of this protection. EPC resulted in robust increase in COX-2 mRNA and PGs levels that were also abrogated by celecoxib.

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Our objective was to characterize adverse cutaneous reactions to celecoxib, a new non steroidal anti-inflammatory drug.