t celebrex dosage
A pure cyclooxygenase-1 inhibitor is probably not indicated as a positive influence on ligament healing but might provide benefits in ligament injury prevention.
Celecoxib is a nonsteroidal anti-inflammatory drug inhibiting enzyme cyclooxygenase-2 (COX-2). The drug was introduced in 1990s. In the work presented here, affinity of celecoxib to enzyme acetylcholinesterase (AChE) is inferred.
celebrex pain medication
Celecoxib may protect against ECS-induced retrograde amnesia by attenuating ECS-induced, COX-2-mediated glutamatergic excitotoxicity.
celebrex 400 mg
50 patients were randomized to either placebo or celecoxib treatment, 200 mg twice daily, for 3 weeks after TKR (NexGen; Zimmer). Maximum total point motion (MTPM) of the tibial component was measured after 2 years using radiostereometric analysis (RSA). In addition, range of motion, pain, and, subjective outcome were evaluated.
celebrex dose rate
COX-2 and NSAIDS differ in their gastrointestinal (GI) and cardiovascular (CV) toxicity from pharmacological, clinical and epidemiologic point of views.
celebrex 90 mg
Thirty-five cases (4.5%) filled prescriptions for cyclo-oxygenase-2 inhibitors within 30 days of the date of upper gastrointestinal bleeding, compared with 79 controls (2.7%). Adjusted odds ratios for upper gastrointestinal bleeding according to prescription for celecoxib, rofecoxib and non-steroidal anti-inflammatory drugs were 1.3 [95% confidence interval (CI), 0.7-2.8], 2.1 (95% CI, 1.2-3.5) and 3.3 (95% CI, 2.4-4.4), respectively.
celebrex dosing instructions
Eighty male Wistar rats were randomly divided into 5 groups: group A, water and normal saline; group B, MNNG and normal saline; group C, MNNG and celecoxib; group D, MNNG and low-dose (1 g/ml) radix curcumae steam distillation extract solution; group E, MNNG and high-dose (2g/ml) radix curcumae wet distillation extract solution. In the end of the 40(th) week, all rats alive were sacrificed and the expressions of VEGF, COX-2 and PCNA in gastric mucosa were determined by immunohistochemistry.
celebrex 2 mg
Tumors in sulindac and celecoxib groups were significantly smaller than those in control group from the second week after drug administration (P<0.01). In treatment group, the cell proliferation index was lower (P<0.05) and apoptosis index was higher (P<0.05) than those in control groups. Compared with the controls, microvessel density was reduced (P<0.01) and expression of CD44v6 on tumor cells was weakened (P<0.05) in treatment groups.
celebrex 800 mg
Our previous studies indicated that while 20 nm particles are rapidly cleared from the periocular space of the rat following posterior subconjunctival injection, 200 nm particles persisted for at least two months. To understand faster clearance of 20 nm particles, the purpose of this study was to determine transscleral permeability and in vivo disposition in the presence and absence of circulation. Further, it was the purpose of this study to simulate sustained retinal drug delivery after periocular administration of rapidly cleared and slowly cleared nanoparticles.
celebrex generic availability
Telomerase and telomerase reverse transcriptase (hTERT) confer cancer cells sustained proliferation and survival potentials. Targeting telomerase or hTERT is a novel anti-cancer strategy. However, telomerase/hTERT inhibition alone has minimal clinical efficacy. We explored the relationship between hTERT and cyclooxygenase 2 (COX2) and evaluated synergistic anti-cancer effects of targeting both hTERT and COX2.
celebrex dose form
Results of previous studies have shown that piroxicam, a cyclooxygenase-1-2 inhibitor, improves the strength of healing ligaments, whereas celecoxib, a cyclooxygenase-2 inhibitor, impairs ligament healing.
Prostaglandins are now known to be produced by Candida albicans and may play an important role in fungal colonization. Their synthesis in mammalian cells is decreased by inhibitors of the cyclooxygenase isoenzymes required for prostaglandin formation. In the present study, a catheter disk model system was used to investigate the effects of nonsteroidal anti-inflammatory drugs (all cyclooxygenase inhibitors) on biofilm formation by three strains of C. albicans. Seven of nine drugs tested at a concentration of 1 mM inhibited biofilm formation. Aspirin, etodolac, and diclofenac produced the greatest effects, with aspirin causing up to 95% inhibition. Celecoxib, nimesulide, ibuprofen, and meloxicam also inhibited biofilm formation, but to a lesser extent. Aspirin was active against growing and fully mature (48-h) biofilms; its effect was dose related, and it produced significant inhibition (20 to 80%) at pharmacological concentrations. Simultaneous addition of prostaglandin E(2) abolished the inhibitory effect of 25 or 50 micro M aspirin. At 1 mM, aspirin reduced the viability of biofilm organisms to 1.9% of that of controls. Surviving cells had a wrinkled appearance, as judged by scanning electron microscopy, and consisted of both yeasts and hyphae. Treatment with other cyclooxygenase inhibitors, such as etodolac, resulted in biofilms that consisted almost entirely of yeast cells. In conventional assays for germ tube formation, these drugs produced significant inhibition, whereas aspirin had little effect. Our findings suggest that cyclooxygenase-dependent synthesis of fungal prostaglandin(s) is important for both biofilm development and morphogenesis in C. albicans and may act as a regulator in these physiological processes. Our results also demonstrate that aspirin possesses potent antibiofilm activity in vitro and could be useful in combined therapy with conventional antifungal agents in the management of some biofilm-associated Candida infections.
We investigated whether celecoxib augments the protective effect of polyethylene glycol (PEG) on colonic aberrant crypt foci (ACF) and tumor formation in F344 rats treated with azoxymethane (AOM). Three groups of rats received AOM: I (AOM alone), II (PEG), and III (PEG/celecoxib). PEG reduced the mean number of total ACF per colon from 190 to 141 (P < 0.05; 26% reduction) and > or = 4-crypt ACF from 95 to 58 (P < 0.01; 39%). Group III rats had a greater proportion of their ACF distally; whereas transverse colon ACF were reduced approximately 50%, distal ACF were reduced by only approximately 8% (P < 0.05). Of 13 large bowel tumors, 8 were in Group I, 4 in Group II, and 1 in Group III rats (P = 0.02). Thus in AOM-treated rats celecoxib appeared to enhance the PEG-induced reduction in colonic tumor formation, and in transverse but not distal or whole-colon ACF.
celebrex dosage 200mg
Thirty New Zealand white rabbits underwent unilateral knee joint surgery using the Hulth technique. Six weeks post-surgery, the animals were randomly divided into three groups, and each group was respectively given weekly intra-articular injections with Celebrex(®), hyaluronic acid and saline. On the sixth week, the results were assessed in rabbit models by gross observation, histological evaluation, and expression of IL-1β, TNF-α, MMP-3.
We examined the involvement of adipocyte cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2)-prostaglandin E receptor (EP)3-mediated signaling during hypertrophy and hypoxia in the development of obesity-associated adipose tissue (AT) inflammation and insulin resistance. The experiments were conducted with high-fat diet (HFD)-induced obese rats, db/db mice, human subjects, and 3T3-L1 and the human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes; the groups were treated with selective inhibitors of COX-2 [celecoxib 30 mg/kg, half maximal inhibitory concentration (IC50) ≈ 0.04 µM] and EP3 (L-798106 100 µg/kg, IC50 ≈ 0.5 µM) or a short interfering RNA. There were strong, positive correlations between adipocyte COX-2 and EP3 gene expressions and the AT TNF-α and monocyte chemotactic protein-1 contents and the homeostatic model assessment for insulin resistance in HFD-induced obese rats, as well as body mass index in human subjects. Treatment with COX-2 and EP3 inhibitors significantly reversed AT inflammatory gene and protein expressions (-50%) and impaired glucose and insulin tolerance in db/db mice. COX-2 inhibition diminished the chemotaxis of adipocytes isolated from HFD rats to macrophages and T cells. Targeting inhibition of adipocyte COX-2 and EP3 during hypertrophy and hypoxia reversed the release of the augmented proinflammatory adipokines and the diminished adiponectin and also suppressed NF-κB and hypoxia-inducible factor-1α transcription activation. These findings suggest that adipocyte COX-2 PGE2-EP3-mediated signaling is crucially involved in the development of obesity-associated AT inflammation and insulin resistance.-Chan, P.-C., Hsiao, F.-C., Chang, H.-M., Wabitsch, M., Hsieh, P. S. Importance of adipocyte cyclooxygenase-2 and prostaglandin E2-prostaglandin E receptor 3 signaling in the development of obesity-induced adipose tissue inflammation and insulin resistance.
These results support the use of GBP in the acute postoperative period. Further trials are needed to delineate the optimal dose, timing and duration of GBP use following surgery.
celebrex maximum dosage
Insufficient studies have been performed to allow a conclusion to be formed with regard to the effectiveness of NSAIDs in the treatment of cachexia in advanced cancer. Major challenges in this patient cohort include the lack of uniformity of inclusion criteria across studies and the frailty of the patients recruited.
celebrex 100 mg
Standardized neuropsychological test battery and statistical parametric mapping (SPM) of FDG-PET scans performed during mental rest.
celebrex cost comparison
Peritonitis induced the increase in the amplitude and frequency of spontaneous contractions. In both distal and proximal colon of the control group, the amplitude of spontaneous contractions was elevated by N(G)-nitro-L-arginine and tetrodotoxin; but the frequency of spontaneous contractions was significantly elevated only in the presence of N(G)-nitro-L-arginine. In both distal and proximal colon of the peritonitis group, the enhanced amplitude and frequency were significantly decreased and returned to control values in the presence of celecoxib.
celebrex y alcohol
The results of this study confirm the clinically relevant antiinflammatory effect of celecoxib at a 200-mg daily dosage, with significant improvement of both pain and function in patients with AS.
celebrex 10 mg
Serious cardiovascular events (CVEs) have been linked to the use of cyclooxygenase (COX)-2 inhibitors, a category of selective NSAIDs. However, few studies are available that have compared the risk for CVEs between COX-2 inhibitors and nonselective NSAIDs in adults undergoing long-term treatment.
celebrex dosing information
Low-dose aspirin (LDA) and nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently prescribed in Japan mostly due to increasing elderly population. Since LDA/NSAIDs cause gastrointestinal injury, serious side effects such as bleeding accompanied with their usage have been frequently reported. Awareness of such problems prompted clinical trials to facilitate a more effective approach to prevent LDA/NSAIDs-induced gastrointestinal ulcer. Two drugs recently approved for health insurance reimbursement, celecoxib, a cyclooxygenase (COX)-2 specific inhibitor and low-dose lansoprazole for prevention of recurrent peptic ulcer due to LDA/NSAIDs will be instrumental in mitigating the gastrointestinal injuries. However, continuous, intensive educational programs will be required to the change in the prescription behaviors of the general physicians. Furthermore, we need to search for effective measures to detect and prevent mid and lower gastrointestinal injury caused by LDA/NSAIDs which account for about 30% of all GI bleedings.
celebrex 400mg capsule
Abnormal angiogenesis is critical for portal hypertension in cirrhosis. Except for etiological treatment, no efficient medication or regime has been explored to treat the early stage of cirrhosis when angiogenesis is initiated or overwhelming. In this study, we explored an anti-angiogenesis effort through non-cytotoxic drugs octreotide and celecoxib to treat early stage of cirrhotic portal hypertension in an animal model. Peritoneal injection of thioacetamide (TAA) was employed to induce liver cirrhosis in rats. A combination treatment of celecoxib and octreotide was found to relieve liver fibrosis, portal venous pressure, micro-hepatic arterioportal fistulas, intrahepatic and splanchnic angiogenesis. Celecoxib and octreotide exerted their anti-angiogenesis effect via an axis of cyclooxygenase-2/prostaglandin E2/EP-2/somatostatin receptor-2, which consequently down-regulated phosphorylation of extracellular signal-regulated kinase (p-ERK)-hypoxia-inducible factor-1α (HIF-1α)-vascular endothelial growth factor (VEGF) integrated signaling pathways. In conclusions, combination of celecoxib and octreotide synergistically ameliorated liver fibrosis and portal hypertension of the cirrhotic rats induced by TAA via the inhibition of intrahepatic and extrahepatic angiogenesis. The potential mechanisms behind the regimen may due to the inactivation of p-ERK-HIF-1α-VEGF signaling pathway.
celebrex generic cost
Celecoxib, rofecoxib, and diclofenac are clinically used cyclooxygenase-2 (COX-2) inhibitors, which have been under intense scrutiny because long-term rofecoxib (Vioxx; Merck, Whitehouse Station, NJ) treatment was found to increase the risk of adverse cardiovascular events. A differential risk profile for these drugs has emerged, but the underlying mechanisms have not been fully elucidated. We investigated the effects of celecoxib, rofecoxib, and diclofenac on ionic currents and calcium signaling in vascular smooth muscle cells (VSMCs) using patch-clamp techniques and fura-2 fluorescence and on arterial constriction using pressure myography. Celecoxib, but not rofecoxib or diclofenac, dramatically enhanced KCNQ (K(v)7) potassium currents and suppressed L-type voltage-sensitive calcium currents in A7r5 rat aortic smooth muscle cells (native KCNQ currents or overexpressed human KCNQ5 currents) and freshly isolated rat mesenteric artery myocytes. The effects of celecoxib were concentration-dependent within the therapeutic concentration range, and were reversed on washout. Celecoxib, but not rofecoxib, also inhibited calcium responses to vasopressin in A7r5 cells and dilated intact or endothelium-denuded rat mesenteric arteries. A celecoxib analog, 2,5-dimethyl-celecoxib, which does not inhibit COX-2, mimicked celecoxib in its enhancement of vascular KCNQ5 currents, suppression of L-type calcium currents, and vasodilation. We conclude that celecoxib inhibits calcium responses in VSMCs by enhancing KCNQ5 currents and suppressing L-type calcium currents, which ultimately reduces vascular tone. These effects are independent of its COX-2 inhibitory actions and may explain the differential risk of cardiovascular events in patients taking different drugs of this class.