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Results for “SALICYLIC ACID”

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At least 1,009 records · Page 56Linked to original sources
PubMed1979

Analgesic activity of diflunisal [MK-647; 5-(2,4-difluorophenyl)salicylic acid] in rats with hyperalgesia induced by Freund's adjuvant.

A method is described for testing analgesia for narcotic or nonnarcotic drugs in rats injected with Freund's adjuvant in the tail, by manipulation of the tail the day after injection, or of the feet after the development of adjuvant arthritis. The method is responsive to a behavioral depressant or an anti-inflammatory steroid. Diflunisal (MK-647; 5-(2,4-difluorophenyl)salicylic acid] exhibited activity in this assay after oral administration with potency about 25 times greater than that of aspirin, about 3 times that of glafenine and twice that of zomepirac. The onset of activity was within a 1/2 hour for narcotic analgesics but required about an hour for non-narcotic compounds. With the latter, the peak of activity was not attained until 2 to 4 hr, depending on the compound. The peak for diflunisal was delayed until the 3rd or 4th hour, but the onset of action was more prompt and the duration greater as the dose was increased. [14C]Diflunisal was concentrated to some extent in the inflamed tissue after adjuvant injection. Peak levels both in plasma and tissue appeared about 2 hr before peak analgesic effect. Repeated administration of large doses produced neither tolerance nor sensitization to the analgesic action of diflunisal. Naloxone and naltrexone did not antagonize the action of the compound, but when morphine and diflunisal were given together, the overall effect was enhanced.

Analgesics↗
PubMed1993

Effects of acetyl salicylic acid and cilostazol administration on serum thrombomodulin concentration in diabetic patients.

Serum thrombomodulin (sTM) is an endothelial cell marker which would reflect the endothelial damage. In order to examine whether some antiplatelet agents decrease the endothelial damage in diabetic patients, sTM concentrations were measured by enzyme-linked immunosorbent assay before and after oral administration of a daily 100 mg of cilostazol for 4 weeks in 9 diabetics or a daily 81 mg of acetyl salicylic acids (ASA) for 4 weeks in 8 diabetics. Basal concentrations of sTM were elevated in most of these patients as compared with healthy subjects. The sTM concentrations were decreased after administration of cilostazol from 28.1 +/- 7.1 ng/ml to 23.6 +/- 5.4 ng/ml (p < 0.01), and after ASA from 30.7 +/- 10.9 ng/ml to 27.9 +/- 11.6 ng/ml (p < 0.05). These results suggest that such drugs can decrease the endothelial damage, resulting in the reduced risk of diabetic vascular complications.

Aged↗
PubMed1993

The ototoxic effect of toluene and the influence of noise, acetyl salicylic acid, or genotype. A study in rats and mice.

Toluene is a widely used organic solvent causing loss of auditory sensitivity in rats and presumably in humans. Also, the hearing loss in humans occupationally exposed to noise has been reported to be aggravated by simultaneous exposure to solvents. The aim of the present investigation was to study the effects of toluene, alone or in combination with other factors, on auditory sensitivity. The influence of acoustic trauma and of acetyl salicylic acid (ASA) on toluene induced auditory sensitivity loss in the rat, as well as the influence on age-related auditory sensitivity loss in two genotypes of mice were studied. An attempt was also made to identify cochlear structures damaged by toluene. Rats or mice were exposed to toluene by inhalation during 1 or 2 weeks. Rats were exposed to noise before or after the toluene exposure, or exposed to ASA by gavage simultaneously with toluene. The effect on auditory sensitivity was measured by frequency specific auditory brainstem response (ABR) between 1.6 and 20 kHz. In the investigations concerning the site of the toluene induced impairment, distortion product otoacoustic emissions (DPOEs) and morphological techniques were used. A permanent loss of auditory sensitivity, as measured by ABR, with the maximal threshold shifts between 6.3 and 12.5 kHz, was found in rats after exposure to toluene. In addition, lowered amplitudes of the DPOEs were recorded, implying that the outer hair cells (OHCs) were affected by toluene. A morphological study confirmed that toluene mainly affects the OHCs. A potentiated loss of auditory sensitivity was seen when toluene had preceded the noise exposure. When the exposure sequence was reversed, i.e. noise preceded toluene, an additive effect was observed. ASA, itself known to cause a reversible auditory impairment, was found to enhance the loss of auditory sensitivity caused by simultaneous toluene exposure. Finally, toluene exposure accelerated the age-related hearing loss in C57BL/6J mice. In conclusion, toluene causes a characteristic mid-frequency auditory damage. The OHCs are particularly susceptible to toluene exposure. The auditory sensitivity loss induced by toluene can be enhanced by ASA and by ensuing noise exposure. Also, toluene exposure can influence the rate of progress of age-related hereditary loss of auditory sensitivity.

Analysis of Variance↗
PubMed1996

Production of Salicylic Acid Precursors Is a Major Function of Phenylalanine Ammonia-Lyase in the Resistance of Arabidopsis to Peronospora parasitica.

Arabidopsis ecotype Columbia (Col-0) seedlings, transformed with a phenylalanine ammonia-lyase 1 promoter (PAL1)-[beta]-glucuronidase (GUS) reporter construct, were inoculated with virulent and avirulent isolates of Peronospora parasitica. The PAL1 promoter was constitutively active in the light in vascular tissue but was induced only in the vicinity of fungal structures in the incompatible interaction. A double-staining procedure was developed to distinguish between GUS activity and fungal structures. The PAL1 promoter was activated in cells undergoing lignification in the incompatible interaction in response to the pathogen. Pretreatment of the seedlings with 2-aminoindan-2-phosphonic acid (AIP), a highly specific PAL inhibitor, made the plants completely susceptible. Lignification was suppressed after AIP treatment, and surprisingly, pathogen-induced PAL1 promoter activity could not be detected. Treatment of the seedlings with 2-hydroxyphenylaminosulphinyl acetic acid (1,1-dimethyl ester) (OH-PAS), a cinnamyl alcohol dehydrogenase inhibitor specific for the lignification pathway, also caused a shift toward susceptibility, but the effect was not as pronounced as it was with AIP. Significantly, although OH-PAS suppressed pathogen-induced lignification, it did not suppress pathogen-induced PAL1 promoter activation. Salicylic acid (SA), supplied to AIP-treated plants, restored resistance and both pathogen-induced lignification and activation of the PAL1 promoter. Endogenous SA levels increased significantly in the incompatible but not in the compatible combination, and this increase was suppressed by AIP but not by OH-PAS. These results provide evidence of the central role of SA in genetically determined plant disease resistance and show that lignification per se, although providing a component of the resistance mechanism, is not the deciding factor between resistance and susceptibility.

Journal Article↗
PubMed1976

Impaired plasma protein binding of phenytoin in uremia and displacement effect of salicylic acid.

The plasma protein binding of phenytoin (DPH) was studied by equilibrium dialysis at 37 degrees C in plasma from uremic patients and healthy subjects. Scatchard plot analyses demonstrated a decreased association constant Ka for the DPH-albumin interaction in the uremic plasma (mean 1.76 - 10(3) M-1 +/-SD 0.12 and a mean 4.10 - 10(3) M-1 +/- SD 0.24 in normal plasma). Studies on separated fractions of serum did not indicate any significant binding of DPH to proteins other than albumin. The nonlinear mathematical relationship between bound DPH and serum albumin could be linearized at low drug concentrations by plotting the ratio of bound/unbound DPH against albumin concentration. The displacement effect of salicylic acid at a concentration of 276 mug/ml (2mM) and DPH was considerable in plasma from normal subjects. In uremic plasma the effect was of much smaller magnitude.

Adult↗
PubMed2007

Synthesis and biological evaluation of quinoline salicylic acids as P-selectin antagonists.

Leukocyte recruitment of sites of inflammation and tissue injury involves leukocyte rolling along the endothelial wall, followed by firm adherence of the leukocyte, and finally transmigration of the leukocyte across cell junctions into the underlying tissue. The initial rolling step is mediated by the interaction of leukocyte glycoproteins containing active moieties such as sialyl Lewisx (sLex) with P-selectin expressed on endothelial cells. Consequently, inhibition of this interaction by means of a small molecule P-selectin antagonist is an attractive strategy for the treatment of inflammatory diseases such as arthritis. High-throughput screening of the Wyeth chemical library identified the quinoline salicylic acid class of compounds (1) as antagonists of P-selectin, with potency in in vitro and cell-based assays far superior to that of sLex. Through iterative medicinal chemistry, we identified analogues with improved P-selectin activity, decreased inhibition of dihydrooratate dehydrogenase, and acceptable CYP profiles. Lead compound 36 was efficacious in the rat AIA model of rheumatoid arthritis.

Administration, Oral↗
PubMed2002

A soybean gene encoding a proline-rich protein is regulated by salicylic acid, an endogenous circadian rhythm and by various stresses.

A cDNA clone of a soybean gene encoding a proline-rich protein (PRP) was characterized and designated SbPRP ( Soy bean Proline- rich Protein). The SbPRP protein is a putative bimodular protein of 126 amino acids with a proline-rich domain and a hydrophobic cysteine-rich domain plus a signal peptide at the N terminal. Southern analysis indicates the presence of a single copy of the SbPRP gene in the soybean genome. The SbPRP gene expression was investigated and the results demonstrate that it accumulates in leaves and epicotyls of soybean seedlings, but not in cotyledons, hypocotyls and roots. The SbPRP mRNA was also expressed in response to salicylic acid and virus infection. In addition, the SbPRP gene transcription was regulated by circadian rhythm, salt stress, drought stress and plant hormones. These results indicate that the SbPRP gene might play a role in plant responses to multiple internal and external factors.

Journal Article↗
PubMed1999

Effects of acetylic salicylic acid and pentoxifylline on the efficacy of intravesical BCG therapy in orthotopic murine bladder cancer (MB49).

PURPOSE: Intravesical immunotherapy with bacillus Calmette-Guerin (BCG), which has become the gold standard in the adjuvant treatment of superficial bladder cancer, is hampered by local side effects. Anti-inflammatory drugs may be helpful, but as an undesired side effect, therapeutic efficacy of BCG might be impaired. Therefore, we investigated the effects of anti-inflammatory drugs on the efficacy of intravesical BCG in an animal model. MATERIALS AND METHODS: Syngenic tumor cells were implanted into the bladders of 75 mice according to our modification of the method. Mice were randomized to 5 groups with 15 animals each and treated with phosphate buffered saline (PBS), group 1; BCG, group 2; BCG + acetylic salicylic acid (ASA), group 3; BCG + pentoxifylline (POF), group 4; autoclaved BCG (aBCG), group 5. Intravesical instillation of 1.35 mg. BCG was initiated one day after tumor inoculation and repeated in weekly intervals for 4 instillations altogether. ASA and POF in doses of 200 mg./kg. and 150 mg./kg., respectively, were given continuously with the drinking water starting at the first instillation. Autoclaved BCG served as control for the importance of viability and was given at the same dose as viable BCG. Mice were monitored for survival, gross hematuria and body weight and after 28 days evaluated for bladder weight and tumor occurrence. RESULTS: Autoclaved BCG and PBS had no effect on tumor growth, whereas animals treated with viable BCG alone and in combination with POF and ASA, respectively, showed a significant reduction in bladder weight: PBS, 248 mg.; BCG, 140 mg. (p = 0.0009); BCG + ASA, 123 mg. (p = 0.0001); BCG + POF, 145 mg. (p = 0.0004); autoclaved BCG, 283 mg. (p = 0.21). Mice treated with BCG, BCG + ASA and BCG + POF showed a significantly higher proportion of survival until day 28 as compared to PBS alone. Autoclaved BCG had no therapeutic efficacy (Kaplan-Meier method/log rank test: BCG, p = 0.0053; BCG + ASA, p = 0.0044; BCG + POF, p = 0.0027; aBCG, p = 0.33). No significant differences among the 3 groups treated with viable BCG, with or without anti-inflammatory drugs, regarding bladder weight and survival were detectable. CONCLUSIONS: The efficacy of BCG therapy in murine orthotopic bladder cancer is dependent on BCG viability and is not compromised by ASA or POF. Clinical trials to evaluate the efficacy of routine ASA or POF to reduce BCG side effects in patients, using self-assessment criteria, should be initiated.

Adjuvants, Immunologic↗
PubMed2003

N-cyanomethyl-2-chloroisonicotinamide induces systemic acquired resistance in arabidopsis without salicylic acid accumulation.

Systemic acquired resistance (SAR) is a potent innate immunity system in plants that is induced through the salicylic acid-mediated pathway. N-cyanomethyl-2-chloroisonicotinamide (NCI) is able to induce a broad range of disease resistance in tobacco and rice and induces SAR marker gene expression without SA accumulation in tobacco. To clarify the detailed mode of action of NCI, we analyzed its ability to induce defense gene expression and resistance in Arabidopsis mutants that are defective in various defense signaling pathways. Wild-type Arabidopsis treated with NCI exhibited increased expression of several pathogenesis-related genes and enhanced resistance to the bacterial pathogen, Pseudomonas syringae pv. tomato DC3000. NCI induced disease resistance and PR gene expression in NahG transgenic plants, but not in the npr1 mutant. NCI could induce PR gene expression in the etr1-1, ein2-1 and jar1-1 mutants. Thus, NCI activates SAR, independently from ethylene and jasmonic acid, by stimulating the site between SA and NPR1.

Arabidopsis↗
PubMed1982

Effects of thrombin, acetyl salicylic acid and prostaglandins on spontaneous efflux of norepinephrine and beta-thromboglobulin from platelets in calcium/magnesium deficient environment.

The effect of different substances on the spontaneous efflux of 14C-norepinephrine (14C-NE) and beta-thromboglobulin (beta TG) from platelets in Ca2+ - and Mg2+ - free buffer was tested. Addition of increasing concentrations of thrombin (0.015-0.625 U/ml) resulted in an immediate increase of 14C-NE detectable in the supernatants, but the slopes of the efflux curves from 10 min after thrombin addition were almost identical and parallel with the slope before thrombin addition. Also beta-thromboglobulin was steadily released after thrombin addition. Prostaglandin E1 and prostacyclin in concentrations that gave a 30-fold increase in cAMP accumulation resulted in a moderate decrease in efflux of 14C-NE from 10 to 30 min but did not influence the efflux thereafter up to 80 min. Acetyl salicylic acid in vivo and in vitro (200-500 mumol/l) did not influence the efflux of 14C-NE or beta TG. The conclusions are that factors known to exert considerable effects on aggregation, desaggregation and acute release produce only transitory effects in a Ca2+ - and Mg2+ - free environment and that the basal efflux of alpha-granule components seems to be a stable process.

Alprostadil↗
PubMed2002

Salicylic acid modulates ozone-induced hypersensitive cell death in tobacco plants.

Ozone-tolerant Bel B and ozone-sensitive Bel W3 tobacco cultivars were subjected to acute ozone fumigation (200 p.p.b. for 3 h) and the subcellular localization of H2O2 was then studied. H2O2 accumulated on the cell walls and plasma membrane of both cultivars but the accumulation pattern differed greatly. H2O2 production was high in both cultivars immediately after fumigation, but, in the tolerant Bel B cultivar, after 7 h was only detected in some spongy cells adjacent to epidermal cells. Instead, in the sensitive Bel W3 cultivar, accumulation was still abundant in the cell walls of palisade, spongy and epidermal cells at this time. Significant changes in apoplastic ascorbate pool were noted in both cultivars in the first hours after fumigation. As the reduced ascorbate content remained unchanged, the marked increase in total ascorbate must have originated from the striking increase in dehydroascorbate, particularly in the ozone-sensitive Bel W3. Exposure of plants to ozone resulted in a marked transient increase in both free and conjugated salicylic acid (SA) as well as an increase in the activity of benzoic acid 2-hydroxylase which catalyses SA biosynthesis. SA induction differed greatly in the two cultivars, in that: (1) SA accumulation was far greater in the ozone-sensitive Bel W3 cv. and (2) the maximum SA peak was delayed in Bel W3 and observed only 7 h after fumigation ended. These results suggest that a high SA content, as documented in the ozone-sensitive Bel W3 cultivar, could trigger the production of ROS with subsequent SA-mediated cell-death.

Journal Article↗