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Neuronal regeneration after damage to an axon tract requires the rapid sealing of the injured plasma membrane and the subsequent formation of growth cones that can lead regenerating processes to their appropriate target. Membrane sealing and growth cone formation are Ca(2+)-dependent processes, but the signaling pathways activated by Ca(2+) to bring about these effects remain poorly understood. An in vitro injury model was employed in which neurites from identified snail neurons (Helisoma trivolvis) were transected with a glass microknife, and the formation of new growth cones from the distal portions of transected neurites was recorded at defined times after transection. This study presents three main results. First, phospholipase A(2) (PLA(2)), a calcium-activated enzyme, is necessary for membrane sealing in vitro. Second, PLA(2) activity is also required for the formation of a new growth cone after the membrane has sealed successfully. Thus, PLA(2) plays a dual role by affecting both growth cone formation and membrane sealing. Third, the injury-induced activation of PLA(2) by Ca(2+) controls growth cone formation through the production of leukotrienes, secondary metabolites of PLA(2) activity. Taken together, these results suggest that the injury-induced Ca(2+) influx acts via PLA(2) and leukotriene production to assure growth cone formation. These findings indicate that events that cause an inhibition of PLA(2) or lipoxygenases, enzymes that produce leukotrienes, could result in the inability of neurites to regenerate.
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Previous studies on the pharmacology of South African medicinal plants in our laboratories and elsewhere have shown that some plants possess therapeutic attributes. One such ethnomedically useful plant is Sutherlandia frutescens R. BR. (family: Fabaceae). S. frutescens is widely used in South African traditional medicine for the management and/or control of a plethora of human ailments. In order to scientifically appraise some of the ethnomedical uses of S. frutescens, the present study was undertaken to investigate the analgesic, antiinflammatory and antidiabetic properties of the plant's shoot aqueous extract in experimental animal models. The analgesic effect of the herb's shoot extract was evaluated using the hot-plate and acetic acid test models of pain in mice, while the antiinflammatory and hypoglycemic effects of the plant's shoot aqueous extract were investigated in rats, using fresh egg albumin-induced pedal (paw) edema, and streptozotocin (STZ)-induced diabetes mellitus. Diclofenac (100 mg/kg) and chlorpropamide (250 mg/kg) were used, respectively, as reference drugs for comparison. S. frutescens shoot aqueous extract (50-800 mg/kg i.p.) produced significant (p < 0.05-0.001) analgesic effects against thermally- and chemically-induced nociceptive pain stimuli in mice. The plant extract (50-800 mg/kg p.o. or i.p.) also significantly (p < 0.05-0.001) inhibited fresh egg albumin-induced acute inflammation and caused significant (p < 0.05-0.001) hypoglycemia in rats. The various chemical constituents and secondary metabolites of the herb are speculated to account for the observed analgesic, antiinflammatory and hypoglycemic effects of the plant. The results of this experimental animal study suggest that S. frutescens shoot aqueous extract possesses analgesic, antiinflammatory, and hypoglycemic properties, and thus lend pharmacological credence to the suggested folkloric uses of the herb in the management and/or control of painful, arthritic and other inflammatory conditions, as well as for adult-onset, type-2 diabetes mellitus in some communities of South Africa.
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Deletion of the cyclooxygenase-2 (COX-2) gene causes impairment of kidney development, but the effect of selective inhibitors of COX-2 (coxibs) or the non-selective inhibitors of COX (the classical non-steroidal anti-inflammatory drugs; NSAIDs) on kidney development was less well described.
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The naturally occurring polymer chitosan was reacted separately with succinic and phthalic anhydrides. The resulting semisynthetic polymers were assessed as potential matrices for colon-specific, orally administered drug delivery. Sodium diclofenac was used as the dispersed model drug. The prepared matrices were incorporated into tablets, which were evaluated in vitro. The evaluation included dissolution studies conducted under simulated gastrointestinal conditions of pH and transit times. The percentage fluid uptake was used to indicate the ability of the matrix to protect an embedded drug from gastric juices. The prepared matrices resisted dissolution under acidic conditions. On the other hand, improved drug release profiles were observed under basic conditions. Therefore, the results suggest the suitability of the prepared matrices in colon specific, orally administered drug delivery system. However, future in vivo testing is planned to fully establish the suitability of the prepared polymers for colon-specific drug delivery.
Mean pupil diameter in the diclofenac group was slightly larger than in the control group, but the difference was not significant. Although mean pupil diameter at the start of surgery was 0.4 mm greater in the diclofenac group, the slopes of regression in pupil diameters were virtually identical between the first three stages of surgery, after which a slight reversal occurred in both groups. The slope of regression of mydriasis was small in both groups.
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Prostaglandins modulate cytokine release though increases in cAMP, regulating interleukin (IL) 6 and IL-10. Diclofenac inhibits cyclo-oxygenase activity and hence prostaglandin production. We hypothesized that diclofenac would affect release of IL-6 and IL-10 and modulate the immune response.
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Total cost of treatment of serious GI adverse effects resulted in an average of $814/patient. Considering the relative risk of such adverse effects for patients with four or more risk factors, the least costly treatment over 6 months was the use of celecoxib ($487). Compared with diclofenac+omeprazole, cost savings were estimated at $59 and $22 per patient with celecoxib and etoricoxib, respectively.
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Transdermal drug delivery influence consumer acceptance and marked increase in bioavailability of some drugs which undergoes hepatic first-pass metabolism. Fabrication of transdermal patch requires lots of attention regarding the amount of components used for it. Because of varied nature of polymer and plasticizer, transdermal patches have different properties and different drug release. This study is on the basis to evaluate the amount to be needed for fabrication of diclofenac transdermal patch. Study shows that Hydroxy Propyl Methyl Cellulose has great influence on transdermal patch, if it is used alone in combination with glycerin or PEG-4000 plasticizer.
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The present, diclofenac-controlled trial concludes that Ayurved Siriraj Wattana Recipe treatment could be an effective treatment of pain in knee OA at 12 weeks.
To evaluate the effectiveness of intramuscular diclofenac in postoperative cesarean section pain control.
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Leech therapy helps relieve symptoms in patients with osteoarthritis of the knee. The potential of leech therapy for treating osteoarthritis and the pharmacologic properties of leech saliva remain to be clarified.
Diclofenac and other non-steroidal anti-inflammatory drugs (NSAIDs) interfere with cyclo-oxygenase-mediated synthesis of prostaglandins, resulting in the inhibition of inflammatory immune responses. In contrast, it is known that NSAIDs are able to induce gastrointestinal damage.
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The searches identified 20 unique RCTs meeting the inclusion criteria: 11 in inflammatory arthritis and 9 in osteoarthritis (OA). The studies included are generally of poor quality. They fall into three main clusters: selenium for rheumatoid arthritis (n = 5); vitamin E for inflammatory arthritis (n = 5) and vitamin E for OA (n = 7). One RCT suggests superiority of vitamin E over placebo and three RCTs suggest equivalence between vitamin E and diclofenac in the treatment of inflammatory arthritis. In OA, four RCTs compared vitamin E with placebo. Two shorter-term studies were positive and two longer-term studies were negative. Two further RCTs suggest equivalence between vitamin E and diclofenac in the treatment of OA. Findings for selenium, vitamin A and a combination product in inflammatory arthritis and for vitamin A, and a combination product in OA were negative. An isolated positive result for vitamin C in OA is of doubtful clinical significance.
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Use of potentially inappropriate medications may result in increased morbidity, mortality and resource utilisation. Due to polypharmacy and age-related decline in renal function the elderly population is at particular risk. Therefore, the Beers Criteria include use of nonsteroidal anti-inflammatory drugs in chronic renal failure stage 4 and 5 as these drugs may worsen renal function. According to the summary of product characteristics, the nonsteroidal anti-inflammatory drugs ibuprofen and diclofenac are contraindicated in these patients. Objective was to assess the extent of nonsteroidal anti-inflammatory drug use in nursing homes with a focus on residents with severe renal failure.
We ranked each NSAID by purchased volume in defined daily doses during September 1996 and compared it with the ranking of gastrointestinal complications from a meta-analysis of controlled epidemiological studies published between 1986 and 1994. We restricted our comparison to those NSAIDs that accounted for 90% of the use and within this DU90% segment we determined the proportion of "high risk" (azapropazone, ketoprofen, piroxicam) and "low risk" (ibuprofen, diclofenac) drugs with respect to gastrointestinal toxicity.
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To develop an effective oral drug delivery system with accelerated absorption in human subjects for a poorly water-soluble acelofenac, five aceclofenac-loaded soft capsule preparations containing various ratios of different solubilizers were prepared and their dissolution tests were carried out. Among five preparations tested, a preparation with ethanolamine was selected as a formula of aceclofenac soft capsule (Korea United Pharm. Co. Ltd., Clanza S, since it was clear in appearance and showed the fastest dissolution rate due to the solubility-enhancing effect of aceclofenac. To evaluate and compare the pharmacokinetics of acelofenac-loaded soft capsules with the conventional aceclofenac tablets (Dae-Woong Pharm. Co. Ltd., Airtal) in human subjects; 14 normal healthy male volunteers (age 20-25 years old) were divided into two groups and a randomized 2 x 2 cross-over study was performed. Following oral administration of one tablet or capsule, each containing 100mg of aceclofenac, blood samples were collected at the predetermined time intervals and the concentration of aceclofenac in plasma was determined by HPLC method using UV detector. The AUC, Cmax, MRT, t1/2 and Kel of aceclofenac delivered from soft capsule were not significantly different from those from aceclofenac-loaded conventional tablet. However, soft capsule gave significantly higher initial concentration and significantly faster Tmax of aceclofenac than did conventional tablet, suggesting that the soft capsule with ethanolamine showed the faster absorption of aceclofenac in human subjects. Thus, the clear aceclofenac-loaded soft capsule with ethanolamine was a more effective oral dosage form with fast absorption for poorly water-soluble aceclofenac.
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Diclofenac can be used up to eight times daily in the rabbit without causing changes in corneal wound healing or epithelial migration rate. There was no significant, long-term reduction of sensitivity, and recovery was not affected by diclofenac.
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Sixty ASA I-II patients (30 in each group) received randomly, and double blindly either ketorolac 0.4 mg.kg-1 or diclofenac 1.0 mg.kg-1 iv after general anaesthesia induction, before surgical incision. In the ketorolac group, the same dose was repeated iv three times at six hour intervals. The diclofenac group patients received diclofenac 1.0 mg.kg-1 after 12 hr iv. Rescue analgesic medication consisting of oxycodone 0.03 mg.kg-1 iv, was administered by a patient controlled analgesia apparatus.
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The Intercontinental Marketing Service Health database was used to determine consumption data between the years 2000 and 2007. We applied the anatomical therapeutical chemical-defined daily dose method, focussing on three major non-steroidal anti-inflammatory drug groups: conventional non-steroidal anti-inflammatory drugs, 'stronger cyclooxygenase 2 inhibitors' (all together as: non-cyclooxygenase 2 selective non-steroidal anti-inflammatory drugs) and selective cyclooxygenase 2 inhibitors. The main outcome measure was defined daily dose/1000 inhabitants/day. Different active agents have been distinguished between the three major groups.
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Irreversible CYP3A inhibition by drugs constitutes one of the major causes of inhibition-based drug interactions. We evaluated time-dependent inactivation of CYP3A in cryopreserved human hepatocytes for six structurally diverse compounds known to exhibit this property. Inactivation kinetic parameters were also determined using human liver microsomes. Except for diclofenac, which did not cause CYP3A inactivation either in microsomes or in hepatocytes at concentrations up to 100 microM, time-dependent inactivation was observed in hepatocytes for amprenavir, diltiazem, erythromycin, raloxifene, and troleandomycin. The observed inactivation potency in hepatocytes (observed IC50) was compared with the potency predicted using microsomal parameters (predicted IC50). Despite satisfactory prediction for troleandomycin (1.35 and 2.14 microM for the predicted and observed IC50, respectively), over-prediction of inactivation was observed for raloxifene, amprenavir, and erythromycin (observed IC50 values 6.2-, 55-, and 7.8-fold higher, respectively, than the predicted IC50). By contrast, the observed IC50 for diltiazem in hepatocytes was approximately 4-fold lower than the IC50 predicted from microsomal data (under-prediction). After correcting for factors including nonspecific binding and inactivator consumption, prediction was significantly improved for raloxifene (the observed IC50 then became 2-fold higher than the predicted IC50) and for amprenavir to a lesser extent. A specific P-glycoprotein inhibitor, 4-(6,7-dimethoxy-3,4-dihydroisoquinolin-2(1H)-yl)-N-[2-(3.4-dimethoxyphenyl)ethyl]-6,7-dimethoxyquinazolin-2-amine (CP-100356), modulated the observed CYP3A inactivation potency by erythromycin and troleandomycin. In summary, these studies reveal three important factors that must be considered when microsomal inactivation parameters are used to predict inhibition-based drug interactions in intact cell systems.
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The present study explored the role of intrinsic mitochondrial membrane potential (delta psi M) in NSAID-induced apoptosis in the early stages of colon cancer. 1,2-Dimethylhydrazine dihydrochloride (DMH) was used to induce colon cancer and its chemoprevention was studied by diclofenac in a rat model. After 6 weeks of treatment with DMH (early stage), morphological analysis revealed a marked occurrence of preneoplastic features [i.e., mucosal plaque lesions (MPLs) in the colonic tissue]. Coadministration of diclofenac with DMH resulted in a significant reduction of these lesions, thereby proving the chemopreventive efficacy of diclofenac at the chosen anti-inflammatory dose. DMH treatment also led to a significant increase in delta psi M in the isolated colonocytes as assessed by JC-1 fluorescent staining, measured both by fluorescence microscopy and spectrofluorometerically. Further, there was seen a reduction in the number of cells showing low delta psi M, and hence monomer intensity of JC-1 by DMH treatment. To study the mechanism of these alterations in delta psi M in the present work, we studied the protein expression of important proapoptotic proteins, cytochrome c and Bax, by Western blot analysis and immunohistochemistry. DMH treatment reduced the mitochondrial translocation of Bax whereas cytochrome c was found to be located prominently in the mitochondria. Protein expression of antiapoptotic Bcl-2 was also studied in the colonic mucosa, which was expectedly found to be overexpressed after DMH treatment. Diclofenac treatment ameliorated the elevated delta psi M and its associated events to exert its chemopreventive action against early stages of colon cancer.
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Because of their frequency, non-opioid analgesics (NOA) single drug exposures registered by Poisons Information Centre (PIC) Erfurt have been studied over a decade.
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The roles of inflammation and immune cell reactivity triggered by amputation have only recently begun to be addressed in investigations of epimorphic regeneration, although studies of tissue repair in mammals clearly show the importance of the immune system in determining the quality of the repair process. Here, we first review inflammation-related work in non-mammalian systems of epimorphic regeneration which suggests that regeneration of an amputated appendage requires continuous modulation of the local immune response, from the first hours after amputation through the period of blastema patterning. We then present data on the effects of anti-inflammatory and proinflammatory agents on regeneration of larval Xenopus hindlimbs. Treatment with the glucocorticoid beclomethasone immediately after amputation inhibits regeneration in regeneration-complete stage 53 limbs. Other anti-inflammatory agents, including the inhibitors of cyclooxygenase-2 (COX-2) activity celecoxib and diclofenac, applied similarly to larvae amputated at stage 55, when the capacity for limb regeneration is normally being lost, restore regenerative capacity. This suggests that although injury-related events sensitive to glucocorticoids are necessary for regeneration, resolution of the inflammatory response may also be required to allow the complete regenerative response and normal blastema patterning. Conversely, if resolution of inflammation is prevented by local treatment of amputated limbs with beryllium, a strong immunoadjuvant, regeneration is inhibited, and gene expression data suggest that this inhibition results from a failure of normal blastema patterning. Both positive and negative effects of immune- or inflammation-related activities occur during anuran limb regeneration and this underscores the importance of considering immune cells in studies of epimorphic regeneration.
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Perioperative use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with risk of anastomotic leak (AL). However, concomitant use of other drugs could infer a bias in risk assessment. Thus, we aimed to interrogate the risk of AL associated with NSAIDs and steroids used perioperatively.
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This study focuses on the complex formed between alpha-cyclodextrin (CD) and the anti-inflammatory drug diclofenac in aqueous solution and also on its potential analytical applications. It was corroborated that the fluorescence emission band of diclofenac is significantly intensified in the presence of alpha-CD. From the changes in the fluorescence spectra, it was concluded that alpha-CD forms a 1:1 inclusional complex with diclofenac and its equilibrium constant was calculated to be 1.20(3)x10(3) M(-1). With the purpose of characterizing the inclusion complex, the acid-base behaviour of diclofenac in both the presence and absence of alpha-CD was spectrophotometrically investigated. From the results obtained, it was inferred that both the carboxyl and the secondary amino groups of the guest molecule remain outside the cyclodextrin cavity. Further details on the complex structure was obtained by (1)H NMR measurements and semiempirical calculations. In addition to the analysis of the alpha-CD-diclofenac interaction, a new approach for the quantification of diclofenac in the presence of alpha-CD is described in the range 0-5 mug ml(-1). An application of the method to the determination of the studied drug in pharmaceutical preparations is shown.
Actinic keratosis (AK) is the most common cutaneous malignant neoplasm and its prevalence continues to increase. According to the most recent findings, AK is currently considered the initial stage, in situ, of squamous cell carcinoma. Field-directed therapies for AKs are the preferred treatment since they have the advantage to clear the clinically visible lesions and also subclinical lesions within the cancerous field. We assessed the cost-effectiveness of topical treatments for AKs including 3% diclofenac in 2.5% hyaluronic acid (HA) gel, imiquimod 5% cream and photodynamic therapy with methyl aminolevulinate (MAL-PDT) in the perspective of the Italian Health Care System (SSN). We used a decision tree analytical approach and efficacy data were drawn from published clinical trials. Cost was evaluated from the SSN perspective during a time horizon of 3 months. A responder was defined as a patient with all lesions clinically cleared and showing an excellent cosmetic result. Based on the applied model, the cost per complete responder was calculated. Diclofenac 3% in HA was less expensive (Euro 256) than MAL-PDT (Euro 320) and imiquimod (Euro 342). Effectiveness was similar and better for diclofenac 3% in HA and MAL-PDT (0.813%) in comparison to 0.734% of imiquimod, respectively. The one-way and probabilistic sensitivity analyses confirmed the results of base case scenario. Based on this cost-effectiveness model, diclofenac 3% in HA can be considered the treatment of choice for AK lesions and surrounding field under a pharmacoeconomic point of view.