• 대한약리학회지
• /
• 제23권1호
• /
• pp.25-31
• /
• 1987

$Cu^{++}$ 촉매작용에 의한 과산화현상이 관절조직손상의 한 형태인 Collagen 손상에 관여할 수 있음을 알아보고, sodium salicylate의 항 염증기전의 일부를 설명해 보고자 sodium salicylate가 이 과산화반응에 미치는 효과를 검토하였다. 쥐피부로 부터 얻은 Collagen을 이용하여 Collagen gelation에 대한 $Cu^{++}$와$H_2O_2$의 효과를 관찰한 결과 $Cu^{++}$ 또는 $H_2O_2$ 단독으로는 gelation에 영향을 미치지 못하였으나, $Cu^{++}$와 $H_2O_2$가 동시에 첨가된 경우 gelation이 억제되어 maximal turbidity가 감소되고, lag phase가 연장됨을 보였다. 그리고 같은 반응 조건에서 sodium salicylate 첨가에 의해 $Cu^{++}$와 $H_2O_2$에 의해 억제된 gelation이 회복됨을 볼 수 있었으며 회복정도는 salicylate 농도 증가에 의존적이었다. 한편 $Cu^{++}$에 의한 $H_2O_2$의 decomposition rate가 sodium salicylate에 의해 증가됨을 보였고, salicylate 농도 증가에 의해 점차 saturation되는 양상을 보였다. 이상의 결과로 부터 $Cu^{++}$ 촉매작용에 의한 과산화 현상은 collagen에 작용하여 구조적 또는 기능적인 변화를 초래함을 알 수 있었고, salicylate에 의해 이러한 과산화 현상이 억제되는 것은 $Cu^{++}$에 의한 $H_2O_2$의 decomposition rate를 증가시킨 결과임을 알 수 있었다. 그러므로 $Cu^{++}$ 촉매작용에 의한 과산화현상은 만성염증 반응 특히 rheumatoid arthritis에서 나타나는 관절조직 손상에 관여할 수 있으며, sodium salicylate는 이 과산화반응에 작용하여 항 염증효과를 나타낼 수 있으리라 믿어졌다.

• 대한의생명과학회지
• /
• 제9권4호
• /
• pp.241-248
• /
• 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.

• 약학회지
• /
• 제28권4호
• /
• pp.217-221
• /
• 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.

• 대한의생명과학회지
• /
• 제23권3호
• /
• pp.290-294
• /
• 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.

• 한방안이비인후피부과학회지
• /
• 제18권1호
• /
• pp.221-233
• /
• 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
• /
• 제10권4호
• /
• pp.230-235
• /
• 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
• /
• 제2권1호
• /
• pp.65-70
• /
• 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.

• 약학회지
• /
• 제44권3호
• /
• pp.263-271
• /
• 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
• /
• 제26권7호
• /
• pp.545-553
• /
• 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.

• 미생물학회지
• /
• 제24권2호
• /
• pp.106-112
• /
• 1986

자연계에서 분리한 Pseudomonas에서 크기가 매우 큰 plasmid (약 180 megadaltons:를 분리하였다. 이 plasmid는 기존의 plasmid 검출방법보다 더 온화한 조건에서 분리되었다. Alkalin., sodium dodecyl sulfate (pH 12. 45)를 사용하여 chromosomal DNA를 변성시킨 뒤 $55^{\circ}C$로 열처리 하여 covalently closed circular DNA 의 손실을 최대한으로 방지하였고, polyethylene glycol을 최종농도 10%로 첨가하여 plasmid DNA를 선택적으로 농축하였다. 한편, 이 plasmid는 mitomycin C를 처리하여 얻은 cured sitrains에서는 나타나지 않아 salicylate를 분해하는 새로운 plasmid로 확인되었다.