• The Korean Journal of Pharmacology
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• v.23 no.1
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• pp.25-31
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• 1987

The present study examines firstly, the inhibition of collagen gelation to explore the possible involvement of $Cu^{++}$-catalyzed peroxidation in rheumatoid arthritis and secondly, the effect of sodium salicylate on this peroxidative reaction to provide a possible explanation for its mechanism of anti-inflammatory action. Incubation of collagen obtained from rat skin with $Cu^{++}$ and $H_2O_2$ resulted in the inhibition of gelation in terms of maximal turbidity and lag phase, but either $Cu^{++}$ or $H_2O_2$ alone essentially gave no effect in the collagen gelation. In the presence of sodium salicylate the inhibited gelation of collagen induced by $Cu^{++}$ and $H_2O_2$ was reversed with the dependency of the concentration of sodium salicylate. Moreover, the rate of $H_2O_2$ decomposition by $Cu^{++}$ was accelerated by sodium salicylate and this decomposition of $H_2O_2$ was found to be saturable in terms of concentration of this drugs. Thus it can be expected that $Cu^{++}$ -catalyzed peroxidation attacks collagen resulting in change of structural or functional integrity of collagen, and sodium salicylate may act on this peroxidative process, possibly through the enhancement of catalatic action of $Cu^{++}$. From these results $Cu^{++}$-catalyzed peroxidation can be in part responsible for degradation of joint tissue in rheumatoid arthritis and sodium salicylate may exert its anti-inflammatory action by this peroxidative reaction.

• Biomedical Science Letters
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• v.9 no.4
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• pp.241-248
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• 2003

Sodium salicylate, a plant stress hormone that plays an important role(s) in defenses against pathogenic microbial and herbivore attack, has been shown to induce a variety of cell responses such as anti-inflammation, cell cycle arrest and apoptosis in animal cells. p38MAPK plays a critical role(s) in the cell regulation by sodium salicylate. However, the signal pathway for sodium salicylate-induced p38MAPK activation is yet unclear. In this study, we show that although sodium salicylate enhances reactive oxygen species (ROS) production, N-acetyl-L-cysteine, a general ROS scavenger, did not prevent sodium salicylate-induced p38MAPK, indicating ROS-independent activation of p38MAPK by sodium salicylate. Sodium salicylate-activated p38MAPK appeared to be very rapidly down-regulated 2 min after removal of sodium salicylate. Interestingly, sodium salicylate-pretreated cells remained fully responsive to re-induction of p38MAPK activity by a second sodium salicylate stimulation or by other stresses, $H_2O$$_2$ and methyl jasmonate (MeJA), thereby indicating that sodium salicylate does not exhibit both homologous and heterologous desensitization. In contrast, pre-exposure to MeJA, $H_2O$$_2$, heat shock, or hyperosmotic stress reduced the responsiveness to subsequent homologous stimulation. Sodium salicylate was able to activate p38MAPK in cells desensitized by other heterologous p38MAPK activators. These results indicate that there is a sensing mechanism highly specific to sodium salicylate for activation of p38MAPK, distinct trom pathways used by other stressors such as MeJA, $H_2O$$_2$ heat shock, and hyperosmotic stress.

• YAKHAK HOEJI
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• v.28 no.4
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• pp.217-221
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• 1984

Nylon microcapsules of sodium salicylate containing three different matrixes, acacia, gelatin and formalized gelatin, were prepared by interfacial polymerization and the effect of the matrix on the dissolution rate of sodium salicylate from its nylon microcapsule was investigated. The microcapsules were spherical and their particle diameter increased in proportion to the amount of matrix. The surface was different from each other according to the kind and the amount of matrix when observed by the scanning electron microscopy. The dissolution rate of sodium salicylate from its microcapsules was decreased by increase of the amount of matrix and the formalized gelatin most decreased the dissolution rate of drugs.

• Biomedical Science Letters
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• v.23 no.3
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• pp.290-294
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• 2017

Metformin or sodium salicylate is known to induce apoptosis and G0/G1 phase arrest in a variety of cancer cells. However, the anti-cancer effects of the combined treatments for these drugs-induced apoptosis are yet unclear. Here, we found that the combined treatment of metformin and sodium salicylate increased the efficacy of chemotherapeutics against breast cancer cells. These combined drugs significantly inhibited cellular proliferation and induced apoptosis at an earlier stage in human MCF-7 breast cancer cells. Also, co-treatments of metformin and sodium salicylate induced G1 cell cycle arrest in MCF-7 cells more effectively than either agent alone. Taken together, these results demonstrate that dual metformin/sodium salicylate treatment prevents proliferation of MCF-7 cells by inducing apoptosis and G1 cell cycle arrest.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.18 no.1
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• pp.221-233
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• 2005

Background and Objectives : Despite of high prevalence, Tinnitus remains obscure because the cause and mechanism is poorly understood. In the absence of a suitable animal model, past investigations tool place in humans. Recently, the animal model with sodium salicylate ototoxicity is broadly used because of its reversibility. Balyangtongum-Tang had been used clinically to treat tinnitus and other hearing problems. We investigated the effects of Balyangtongum-Tang on cochlear morphologic change induced by sodium salicylate ototoxicity and were to find out its therapeutic effects on ototoxicity in rat model. Materials and Methods : Healthy ten Sprague-Dawley rats were divided into normal(2), control(4) and sample(4) groups. The sample group was given extract of Balyangtongum - Tang(1cc/100g) once a day for 4 days. After 3 hours when last medication were given, the sample and control groups were injected intraperitoneally with sodium salicylate(500mg/kg). We observed the cochlear morphologic changes of rats every 1, 2, 3 and 5 hours after injection. Results : The electron microscopic finding of outer hair cell shows some changes in the curticular plate and cytoplasm. Some vacuoles were found in the control and sample groups. Vacuolization in the curticular plate and cytoplasm of the sample group after 3, 5 hours were similar to the control group. But the curticular plate of the sample group after 1, 2 hours did not from vacuole. On the other hand the control group after 1, 2 hours formed vacuoles in the curticular plate. Light microscopic findings of cochlear duct in control and sample groups didn't find any difference. Conclusion : The results suggest that extract of Balyangtongum-Tang reduces the morphologic changes induced by sodium salicylate ototoxicity and the effects are remarkable in frist 2 hours. However the effective times are different with previous studies, it seems to due to the difference of tolerance and sensitivity of laboratory animals.

• Biomolecules & Therapeutics
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• v.10 no.4
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• pp.230-235
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• 2002

Gold sodium thiomalate (GST, gold compound) is a widely used anti-arthritic, anti-rheumatic and anti-inflammatory drug that is considered a good alternative to sodium salicylate (NaSA) for individuals who cannot tolerate salicylates. Nitric oxide (NO) synthesized by inducible nitric oxide synthase (iNOS) has been implicated as a mediator of inflammation. Recent evidence suggests that anti-inflammatory effect of NaSA lies in the inhibition of iNOS, but nothing has been reported about the direct effect of iNOS expression by GST. The present study was designed to elucidate sequentially the action mechanisms of GST and NaSA on lipopolysaccharide (LPS) plus interferon-gamma (IFN-$\gamma$) induced iNOS expression in RAW 264.7 macrophages. Both GST and NaSA inhibited NO production and iNOS protein expression in a dose dependent manner. GST inhibited iNOS mRNA expression induced by LPS plus IFN-$\gamma$, whereas NaSA did not. These findings suggest that GST may exert anti-arthritic, anti-rheumatic and anti-inflammatory effect by inhibiting iNOS expression induced by LPS plus IFN-$\gamma$ at transcriptional level, whereas NaSA exert its effect by inhibiting iNOS expression at the translational or posttranslational level.

• Archives of Pharmacal Research
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• v.2 no.1
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• pp.65-70
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• 1979

Distribution and binding properties of sodium salicylate the human red blood cells were studied under various experimental conditions. The effect of tonicity and hemolysis on the steady state level of the drug within the human red blood cells were accounted for in this study. When the washed cells were suspended in normal saline solution, the drug was so rapidly permeated into red cells. Since the pH of the system forces nearly complete ionization of the drug, ionic diffusion through aqueous pores is thought to be the mode of salicylate transport. Human red cell binding capacity and association constant for salicylate were estimated. This work supports the view that the red cells act asan important reservior of salicylate.

• YAKHAK HOEJI
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• v.44 no.3
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• pp.263-271
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• 2000

In an attempt to develop an injectable form of practically insoluble biphenyl dimethyl dicarboxylate (DDB), the effect of various vehicles, cosolvents and hydrotropic agents was investigated. It was found that polyethylene glycol (PEG) 400 revealed the best solvency toward DDB (17.7 mg/ml at $37^{\circ}C$), and decreasing order of the solubility was as follows: PEG 400>PEG 300>diethylene glycol monoethyl ether (DGME)>PEG-8 glyceryl caprylate/caprate. Among the hydrotropes used, sodium salicylate, sodium benzoate and nicotinamide were effective in increasing the solubility in water. The solubility of DDB in 2 M sodium salicylate, sodium benzoate and nicotinamide solutions was increased 44.3, 23.5 and 44.0 times than that in water, respectively. The addition of sodium salicylate and sodium benzoate to PEG 300-water PEG 400-water and DGME-water cosolvents remarkably increased the solubility of DDB, and significantly retarded precipitate formation when mixed with water Hemolytic properties of DDB injections (2 mg/4~10 ml) in PEG 300-water or DGME-water (60:40 v/v) cosolvents containing sodium benzoate (0.14~0.35 M) were very low. It was concluded from the results that these solutions would be applied to the design of new DDB injections.

• Archives of Pharmacal Research
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• v.26 no.7
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• pp.545-553
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• 2003

The expression of cyclooxygenase-2 (COX-2) is a characteristic response to inflammation, which can be inhibited with sodium salicylate. IL-1$\beta$ and TNF-$\alpha$ can induce extracellular signal-regulated kinase (ERK), IKK, IkB degradation and NF-$\kappa$B activation. Salicylate inhibited the IL-1$\beta$ and TNF-$\alpha$-induced COX-2 expressions, regulated the activation of ERK, IKK and IkB degradation, and the subsequent activation of NF-$\kappa$B, in neonatal rat ventricular cardiomyocytes. The inhibition of the ERK pathway, with a selective inhibitor, PD098059, blocked the expressions of IL-1$\beta$ and TNF-$\alpha$-induced COX-2 and $PGE_2$ release. The antioxidant, N-acetyl-cysteine, also reduced the glutathione or catalase- attenuated COX-2 expressions in IL-1$\beta$ and TNF-$\alpha$-treated cells. This antioxidant also inhibited the activation of ERK and NF-$\kappa$B in neonatal rat cardiomyocytes. In addition, IL-1$\beta$ and TNF-$\alpha$-stimulated the release of reactive oxygen species (ROS) in the cardiomyocytes. However, salicylate had no inhibitory effect on the release of ROS in the DCFDA assay. The results showed that salicylate inhibited the activation of ERK and IKK, I$\kappa$B degradation and NF-$\kappa$B activation, independently of the release of ROS, which suggested that salicylate exerts its anti-inflammatory action through the inhibition of ERK, IKK, IkB and NF-$\kappa$B, and the resultant COX-2 expression pathway in neonatal rat ventricular cardiomyocytes.

• Korean Journal of Microbiology
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• v.24 no.2
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• pp.106-112
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• 1986

The large plasmid (about 180 megadaltons) was isolated from the aquatic strain of Pseudomonas which was found to degrade salicylate. It was found that the plasmid could be isolated under gentle conditions in comparison with other methods. The yield of covalently closed circular DNA was enganced by heat treatment at $55^{\circ}C$ after denaturing the chromosomal DNA with alkaline sodium dodecyl sulfate (pH 12.45), and the plasmid DNA was selectively concentrated by utilizing 10% polyethylene glycol as final concentration. It was also found that the cured strains with mitomycin C did not show any growth on the medium containing salicylat6e, therefore, it was concluded that the plasmid might play and important role on the salicylate degradation.