In irritated eyes, 72 h of meloxicam treatment downregulated COX-2 expression and activity (mRNA by RT-PCR and PGE2 levels by ELISA, respectively) in a time-dependent manner and reduced inflammation. Meanwhile, diclofenac failed to reduce COX-2 mRNA or PGE2 to basal levels after 7 days of treatment. Meloxicam treatment downregulated IL-6 and IFN-gamma expression in the conjunctiva and IL-1beta and TNF-alpha expression in the cornea. Diclofenac failed to modify these cytokines in both tissues. Meloxicam treatment increased the expression of IL-6 in conjunctiva, and IL-10 in cornea, while diclofenac had no effect on these cytokines.
The data indicate that I/R results in the modification of the levels of several gene transcripts involved in GABAergic signalling in both the pre- and postsynaptic components, of this neurotransmitter system, in an age- and structure-dependent manner.
Pain alleviation associated with castration of piglets is an important welfare issue. The present study compares the effect of different approaches and products suitable for farmer use, with the aim to alleviate pain due to castration in piglets. A randomized within-litter design, with 28 replicate litters, compared 7 treatments: handling () restraint of the piglet and manipulation of the scrotum, castration without pain relief (), 2 treatments (, ) with different concentrations of tetracaine (2 and 6%) applied topically 10 min before and immediately post-surgery, and 3 treatments with i.m. injection of different nonsteroidal anti-inflammatory drugs () 10 min prior to surgery (-meloxicam, -ketoprofen, -tolfenamic acid). Efficacy of pain relief was assessed during a 300 min period after castration by serum cortisol, behavior (walking, lying, suckling, in the nest, isolated and pain related: tremors, rubbing the rear, hunching, wagging of the tail), facial expression and scrotal skin pressure sensitivity. C pigs had greater serum cortisol concentration than all other groups at 60 min post-surgery ( < 0.001), while H pigs had lower concentrations than pigs given topical anesthesia ( < 0.001) though not injected analgesia. No treatment differences were significant at 180 min, but at 300 min cortisol concentration was greater in T2 and T6 piglets than those given NSAIDs ( = 0.03). These treatment differences were mirrored by the pressure sensitivity of the scrotum; in comparison with C piglets, those given NSAIDs showed a reduced sensitivity ( 0.003) but those given local anesthesia did not ( = 0.15). C pigs showed increased frequency of pain-related behavior in the first 30 min in comparison with all other treatments, more time isolated than H or NSAID treatments, and more time standing inactive than H or K treatments. No behavioral differences were apparent after 60 min. No differences in facial expressions were observed among treatments. In conclusion, on-farm methods for pain relief can provide some, though not complete, pain alleviation in the hours after castration. The use of topical anesthesia gave only minor benefit in comparison to NSAID agents injected prior to castration. Since the main differences in indicators of pain between positive and negative controls were observed within the first h after castration, it is important to select drugs that act quickly after administration to facilitate practical processing schedules on farm.
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The effect of 21 days of repeated oral administration of levofloxacin and enrofloxacin both alone and in combination with meloxicam, on the oxidative balance in blood was evaluated in rabbits. Rabbits were randomly allocated to six groups of four animals each. Control group was gavaged 5% dextrose and 2% benzyl alcohol. Three groups were exclusively gavaged meloxicam (0.2 mg/kg body weight o.d.), levofloxacin hemihydrate (10 mg/kg body weight b.i.d 12 h), and enrofloxacin (20 mg/kg body weight o.d.), respectively. Two other groups were co-gavaged meloxicam with levofloxacin hemihydrate and enrofloxacin, respectively. A reduction (p < 0.05) of reduced glutathione levels was observed in groups treated with meloxicam both alone and in combination with levofloxacin, whereas an increase (p < 0.01) in the levels of this antioxidant was observed in the groups treated with enrofloxacin. The activities of enzymes, glutathione peroxidase and superoxide dismutase, were induced (p < 0.05) in levofloxacin-alone treated group. Superoxide dismutase was also induced (p < 0.05) in meloxicam-alone treated group and inhibited (p < 0.05) in enrofloxacin-meloxicam co-treated group. The activity of catalase was non-significantly different between various groups. Enrofloxacin-treated groups had higher (p < 0.01) lipid peroxidation than control and levofloxacin-alone treated groups. Elevated lipid peroxidation was also observed in the groups treated with meloxicam both alone and in combination with levofloxacin (p < 0.05). In conclusion, these drugs have potential to induce oxidative imbalance, however, compared to levofloxacin, more oxidative damage is produced by enrofloxacin and meloxicam.
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Intergroup comparisons demonstrated that meloxicam significantly reduced bone healing around implants. For zone A, significant differences were observed regarding BIC (47.01 +/- 10.48 A; 35.93 +/- 12.25 B), BA (86.42 +/- 3.66 A; 61.58 +/- 12.09 B), and BD (96.86 +/- 0.96 A; 91.06 +/- 3.05 B) for control and test groups, respectively (P <0.05). For zone B, data analysis also showed significant differences among groups for BIC (30.76 +/- 13.80 A; 16.86 +/- 11.48 B), BA (34.83 +/- 8.18 A; 25.66 +/- 9.16 B), and BD (15.76 +/- 7.05 A; 7.73 +/- 4.61 B) for control and test groups, respectively (P <0.05).
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Necropsy and histological examination revealed a severe pneumonia, with numerous Angiostrongylus mackerrasae in the pulmonary artery. The pulmonary parenchyma contained numerous eggs and rare larvae.
The use of proton pump inhibitors or misoprostol is known to prevent the gastrointestinal complications of nonsteroidal anti-inflammatory drugs (NSAIDs). Rebamipide is known to increase the mucosal generation of prostaglandins and to eliminate free oxygen radicals, thus enhancing the protective function of the gastric mucosa. However, it is unknown whether rebamipide plays a role in preventing NSAID-induced gastropathy. The aim of this study was to determine the effectiveness of rebamipide compared to misoprostol in preventing NSAID-induced gastrointestinal complications in patients requiring continuous NSAID treatment.
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Monoarthritis was induced (for behavioural studies) by injection of complete Freund's adjuvant into the ankle. Meloxicam was given for 5 days (0.1-4 mg/kg/ day i.p.). Inflammation of the knee or paw (for electrophysiology) was induced with carrageenan. Meloxicam was given i.v. (4-64 mg/kg).
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15 healthy ball pythons.
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Diclofenac and rofecoxib had higher rates of aminotransferase elevations than placebo and other NSAIDs studied. No NSAID studied had increased rates of liver-related serious adverse events, hospitalizations, or deaths.
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Evaluate the antinociceptive effects of subarachnoid meloxicam on the mechanical hypernociception induced by carrageenan in rats.
Pain scores were very low at 24 hours after surgery in the context of multimodal analgesia and were not improved by additives. However, perineural buprenorphine and dexamethasone prolonged block duration, reduced the worst pain experienced, and reduced opioid use. Intravenous buprenorphine caused troubling nausea and vomiting. Future research is needed to confirm and extend these observations.
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The COX-2 protein is frequently overexpressed in human malignant gliomas. This expression has been associated with their aggressive growth characteristics and poor prognosis for patients. Targeting the COX-2 pathway might improve glioma therapy. In this study, the effects of the selective COX-2 inhibitor meloxicam alone and in combination with irradiation were investigated on human glioma cells in vitro. A panel of three glioma cell lines (D384, U87 and U251) was used in the experiments from which U87 cells expressed constitutive COX-2. The response to meloxicam and irradiation (dose-range of 0-6 Gy) was determined by the clonogenic assay, cell proliferation was evaluated by growth analysis and cell cycle distribution by FACS. 24-72 h exposure to 250-750 microM meloxicam resulted in a time and dose dependent growth inhibition with an almost complete inhibition after 24 h for all cell lines. Exposure to 750 microM meloxicam for 24 h increased the fraction of cells in the radiosensitive G(2)/M cell cycle phase in D384 (18-27%) and U251 (17-41%) cells. 750 microM meloxicam resulted in radiosensitization of D384 (DMF:2.19) and U87 (DMF:1.25) cells, but not U251 cells (DMF:1.08). The selective COX-2 inhibitor meloxicam exerted COX-2 independent growth inhibition and radiosensitization of human glioma cells.
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The treatment of animals with meloxicam or diclofenac (2.8-94.3 micromol/kg, i.p. 30 min prior) caused graded and significant inhibition of AA, with mean ID50 values of 7.4 and 38.0 micromol/kg, respectively. At the ID50 level, meloxicam was about 5-fold more potent than diclofenac. In the formalin test, meloxicam or diclofenac (0.8-94.3 micromol/kg, i.p. 30 min prior) also caused significant inhibition of both the early (neurogenic pain) and the late (inflammatory pain) phases of formalin-induced licking. The calculated mean ID50 values for the early phase were: 7.1 and > 94.3 micromol/kg, while for the late phase they were 2.8 and 34.5 micromol/kg, respectively, for meloxicam and diclofenac. Meloxicam also caused significant inhibition of formalin-induced oedema (p < 0.05). Meloxicam and diclofenac (0.8-314.4 micromol/kg, i.p. 30min prior) produced significant and dose-related inhibition of neurogenic nociception caused by topical injection of capsaicin, with mean ID50 values of 4.0 and 47.4 micromol/kg, respectively, but were ineffective in the hot-plate model of nociception.
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To describe a method to study joint pain in experimental osteoarthritis (OA) and to study nitric oxide (NO) participation in experimental OA.
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Human serum albumin (HSA) is the most prominent protein in plasma. The three-domain design of HSA provides a variety of binding sites for many ligands, including heme, bilirubin and drugs. Here, we report the effect of new generation, non-steroidal anti-inflammatory drug (NSAID) meloxicam on the albumin conformation and ligand binding. In the present work the interaction of meloxicam with HSA in aqueous solution at physiological pH has been investigated through circular dichroism and fluorescence spectroscopy. The strong quenching of the fluorescence clearly indicated that the binding of the drug to HSA changed the microenvironment of tryptophan residue and the tertiary structure of HSA. This was confirmed by the destabilization of the warfarin binding site. CD and fluorescence spectroscopic results showed marked reductions (about 40% decrease in the CD Cotton effect intensity, and approximately 15% decrease of the fluorescence intensity) in the affinity of albumin for bilirubin upon meloxicam binding. The strong inhibition of warfarin and ANS bound to protein after meloxicam modification compared with aspirin confirms that the binding site of both drugs is not the same.
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An article highlights the pathogenetic aspects of treatment of reflex pain syndromes in the degenerative-dystrophic spinal lesions. Attention is focused on a rational combination of medications that may shorten the duration of analgesic and anti-inflammatory therapy to prevent the development of side-effects caused by non-steroid anti-inflammatory medications. The results of own research of analgesic efficacy and tolerability of treatment in 50 patients with chronic skeletal-muscle pain syndromes in the state of exacerbation assigned to the combination of a non-steroid anti-inflammatory medication mesipol (meloxicam) with a central myorelaxant baclosan (baclofen) are discussed. It was found the positive effect of therapy not only on pain syndrome but on comorbid symptoms as well.
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Lyme neuroborreliosis (LNB), caused by the spirochete Borrelia burgdorferi (Bb), could result in cognitive impairment, motor dysfunction, and radiculoneuritis. We hypothesized that inflammation is a key factor in LNB pathogenesis and recently evaluated the effects of dexamethasone, a steroidal anti-inflammatory drug, and meloxicam a non-steroidal anti-inflammatory drug (NSAID), in a rhesus monkey model of acute LNB. Dexamethasone treatment significantly reduced the levels of immune mediators, and prevented inflammatory and/or neurodegenerative lesions in the central and peripheral nervous systems, and apoptosis in the dorsal root ganglia (DRG). However, infected animals treated with meloxicam showed levels of inflammatory mediators, inflammatory lesions, and DRG cell apoptosis that were similar to that of the infected animals that were left untreated.
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Pancreaticobiliary maljunction (PBM) is a high risk factor in biliary tract carcinoma. The chemopreventive action of a cyclooxygenase (COX)-2 inhibitor (meloxicam) on N-nitrosobis (2-oxopropyl) amine (BOP)-induced gallbladder cancer in hamster PBM models was investigated. In 7-week-old female Syrian golden hamsters, the extrahepatic bile duct at the distal end of the common duct was ligated and cholecystoduodenostomy was performed (group I). In group II, the same surgery was performed and from week 4 after surgery, 10 mg/kg of BOP was injected subcutaneously once a week with a 1-week interval. In group III, in addition to the measures employed in group II, 5 mg/kg/day of meloxicam was administered once a day, every weekday. Pathological findings in the gallbladder in week 20 after surgery were as follows. In group I, proper epithelium (PE) was predominant and there was no cancer. In group II, PE was predominant, but there was also hyperplasia and atypical epithelium (AE) recognized in 8 of 11 cases (72.7%); the area of AE was more extensive than that in group I. Carcinoma in situ (CIS) was recognized in 4 of 11 cases (36.4%) in group II. Group III showed the same pathological findings as group I. However, compared with group II, the incidence of AE decreased to 27.3% and no cancerous lesion was observed. In week 20 after surgery, the proliferative cell nuclear antigen labeling index in group III was statistically significantly lower than in group II (P = 0.045). No statistically significant differences were noted among the groups in terms of apoptosis labeling index in week 20 after surgery. In conclusion, it was confirmed that meloxicam suppresses carcinogenesis in hamster PBM models and its mechanism may be based on the suppression of cell growth.
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Intra-subject variation for COX-1 and COX-2 at baseline was at 26 +/- 18% and 18 +/- 13% respectively, and intersubject variation at 39% and 36%, respectively. The ratios of IC50s and, at best, of IC80s revealed diclofenac and meloxicam as selective COX-2 inhibitors and ibuprofen as a preferential COX-1 inhibitor in vitro. However, after oral intake, ibuprofen inhibited ex vivo COX-2 by 80% whereas diclofenac inhibited COX-1 by 70%. Meloxicam inhibited COX-1 from 30 to 55% depending on the repetition of the dose and increase in plasma concentrations. Using in vitro dose--response curves, the in vivo inhibitory potency of diclofenac was estimated adequately from its circulating concentration ([-0.18, 0.21] for COX-1 and [-0.13, -0.03] for COX-2) but this was not the case for ibuprofen on COX-2 ([-0.14, 0.27]) and meloxicam on COX-1 ([0.31, 1.05]). The limited predictability of the system was not improved through considering the unbound fraction of the drugs or the variable chiral inversion of ibuprofen.