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Sodium salicylate

CAS# 54-21-7

Sodium salicylate

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Chemical structure

Sodium salicylate

3D structure

Chemical Properties of Sodium salicylate

Cas No. 54-21-7 SDF Download SDF
PubChem ID 16760658 Appearance Powder
Formula C7H5NaO3 M.Wt 160.1
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Salicylic acid sodium salt; 2-Hydroxybenzoic acid sodium salt
Solubility H2O : ≥ 100 mg/mL (624.61 mM)
DMSO : 100 mg/mL (624.61 mM; Need ultrasonic)
*"≥" means soluble, but saturation unknown.
Chemical Name sodium;2-hydroxybenzoate
SMILES [Na+].Oc1ccccc1C([O-])=O
Standard InChIKey ABBQHOQBGMUPJH-UHFFFAOYSA-M
Standard InChI InChI=1S/C7H6O3.Na/c8-6-4-2-1-3-5(6)7(9)10;/h1-4,8H,(H,9,10);/q;+1/p-1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Sodium salicylate

DescriptionSodium Salicylate inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation.In Vitro:Sodium Salicylate is an effective inhibitor of COX-2 activity at concentrations far below those required to inhibit NF-κB (20 mg/mL) activation. Sodium Salicylate inhibits prostaglandin E2 release when add together with interleukin 1β for 24 hr with an IC50 value of 5 μg/mL, an effect that is independent of NF-κB activation or COX-2 transcription or translation. Sodium Salicylate acutely (30 min) also causes a concentration-dependent inhibition of COX-2 activity measured in the presence of 0, 1, or 10 μM exogenous arachidonic acid. In contrast, when exogenous arachidonic acid is increased to 30 μM, Sodium Salicylate is a very weak inhibitor of COX-2 activity with an IC50 of >100 μg/mL. When added together with IL-1β for 24 hr, Sodium Salicylate causes a concentration-dependent inhibition of PGE2 release with an apparent IC50 value of approximately 5 μg/mL. The ability of Sodium Salicylate to directly inhibit COX-2 activity in A549 cells is tested after a 30-min exposure period, followed by the addition of different concentrations of exogenous arachidonic acid (1, 10, and 30 μM). Sodium Salicylate causes a concentration-dependent inhibition of COX-2 activity in the absence of added arachidonic acid or in the presence of 1 or 10 μM exogenous substrate with an apparent IC50 value of approximately 5 μg/mL. However, when the same experiments are performed using 30 μM arachidonic acid, Sodium Salicylate is an ineffective inhibitor of COX-2 activity, with an apparent IC50 value of more than 100 μg/mL, and achieves a maximal inhibition of less than 50%[1].In Vivo:In C57Bl/6 DIO mice, Salicylate decreases both fasting and postprandial plasma glucose levels. Furthermore, there is a trend to reduce plasma triglyceride levels after Salicylate treatment in C57Bl/6 DIO mice (P=0.059). Salicylate significantly reduces 11β-HSD1 mRNA in omental adipose tissue in C57Bl/6 DIO mice, with a similar trend in mesenteric adipose (P=0.057). In mesenteric adipose of C57Bl/6 DIO mice, Salicylate also reduces 11β-HSD1 enzyme activity[2].

References:
[1]. Mitchell JA, et al. Sodium salicylate inhibits cyclo-oxygenase-2 activity independently of transcription factor (nuclear factor kappaB) activation: role of arachidonic acid. Mol Pharmacol. 1997 Jun;51(6):907-12. [2]. Nixon M, et al. Salicylate downregulates 11β-HSD1 expression in adipose tissue in obese mice and in humans, mediating insulin sensitization. Diabetes. 2012 Apr;61(4):790-6.

Protocol

Kinase Assay [1]
Human purified COX-2 are and the cofactors Glutathione (5 mM), Adrenaline (5 mM), and Hematin (1 μM) are dissolved in 50 mM Tris buffer (pH 7.5). Hematin is first dissolved in a concentrated stock of 100 mM in 1 M NaOH before being further diluted in Tris buffer. Enzyme reactions are carried out in individual wells of 96-well plates with a final reaction volume of 200 μL. Different concentrations of Sodium Salicylate are added to the plate, followed by the addition of 10 units of enzyme (180 μL). The plates are incubated at 37° for 30 min before Arachidonic acid (10 nM to 30 μM) is added for a further 15 min. The reaction is stopped by heating the plate to 100°C for 5 min. The 96-well plate is then centrifuged at 10,000 × g for 10 min, and appropriated samples are removed and added into the radioimmunoassay[1].

Cell Assay [1]
To assess the direct effect of Sodium Salicylate on COX-2 activity after induction has occurred, A549 cells are first treated with IL-1β for 24 hr, and the culture medium is replaced with DMEM containing different concentrations of Sodium Salicylate(10, 100 and 1000 μg/mL). Cells are incubated at 37°C for 30 min. Arachidonic acid (1-30 μM) is then added for 15 min, and the medium is removed for the measurement of PGE2[1].

Animal Administration [2]
Mice[2] Adult male C57Bl/6 mice are at age 12 weeks. Diet-induced obese C57Bl/6 mice (C57Bl/6 DIO) are given 10 weeks of high-fat diet (58% fat, 12% sucrose) before treatment. Sodium Salicylate (120 mg/kg/day) or distilled water (vehicle) is administered from 1 week after arriving (C57Bl/6 Lean), after 10 weeks of high-fat feeding (C57Bl/6 DIO), or after achieving target weight (HSD1KO-DIO) for 4 weeks to groups of n=8 via osmotic minipumps implant subcutaneously between the scapulae.

References:
[1]. Mitchell JA, et al. Sodium salicylate inhibits cyclo-oxygenase-2 activity independently of transcription factor (nuclear factor kappaB) activation: role of arachidonic acid. Mol Pharmacol. 1997 Jun;51(6):907-12. [2]. Nixon M, et al. Salicylate downregulates 11β-HSD1 expression in adipose tissue in obese mice and in humans, mediating insulin sensitization. Diabetes. 2012 Apr;61(4):790-6.

Sodium salicylate Dilution Calculator

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Sodium salicylate Molarity Calculator

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Preparing Stock Solutions of Sodium salicylate

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 6.2461 mL 31.2305 mL 62.461 mL 124.9219 mL 156.1524 mL
5 mM 1.2492 mL 6.2461 mL 12.4922 mL 24.9844 mL 31.2305 mL
10 mM 0.6246 mL 3.123 mL 6.2461 mL 12.4922 mL 15.6152 mL
50 mM 0.1249 mL 0.6246 mL 1.2492 mL 2.4984 mL 3.123 mL
100 mM 0.0625 mL 0.3123 mL 0.6246 mL 1.2492 mL 1.5615 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Sodium salicylate

Sodium salicylate is a metabolite of acetylsalicylic acid, and functions by inhibiting NF-kB and reduces oxidative stress.

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References on Sodium salicylate

The role of the binding salt sodium salicylate in semidilute ionic cetylpyridinium chloride micellar solutions: a rheological and scattering study.[Pubmed:27929164]

Phys Chem Chem Phys. 2016 Dec 21;19(1):782-790.

The micellar system based on cetylpyridinium chloride (CPyCl) and Sodium salicylate (NaSal) in brine solution is investigated on both macro- and micro-length scales through rheology and scattering measurements. The linear viscoelasticity of the system and its structural parameters are explored by systematically changing the amount of NaSal over an extremely wide range of concentrations, thus producing salt-to-surfactant molar ratios from zero to about 8.5. As a result, the well-known non-monotonic behaviour of the zero-shear rate viscosity as a function of salinity can be connected to micellar morphological changes, whose driving force is represented by the simultaneous binding and screening actions of NaSal. The viscosity behaviour can be seen as a direct consequence of consecutive lengthening/shortening of the contour length, where the micelles attempt to minimize the electrostatic charge density on their surface. Along similar lines, the scattering measurements of the semidilute solutions show that the local stiffness of the micellar chain changes with increasing salt content influencing the elasticity of the resulting network. Within this general view, the branching of the micelles can be seen as a side effect attributable to the main character of the play, namely, the binding salt NaSal, whereas the overall dynamics of the system is driven by the considerable changes in the entanglement density of the micellar network.

Short communication: Sodium salicylate negatively affects rumen fermentation in vitro and in situ.[Pubmed:28088410]

J Dairy Sci. 2017 Mar;100(3):1935-1939.

Administration of Sodium salicylate (SS) to cows in early lactation has a positive effect on whole-lactation milk production but a negative effect on metabolism in some cases. The objective of this trial was to determine whether SS directly affects rumen fermentation. Experiment 1 was designed to investigate the effects of direct inclusion of SS in a 24-h batch culture, and experiment 2 was designed to test the fermentative ability of rumen fluid from heifers who had received SS. In experiment 1, we combined strained and pooled rumen fluid from 3 heifers in a 2:1 ratio with McDougall's buffer, and added 150 mL of the inoculum to each flask (n = 5/treatment) with 2.5 g of fermentation substrate similar to a lactating cow ration, ground to 1 mm. We then added premixed treatments (1-mL volume) to achieve the desired final amount of SS (CON1 = 0 mg, LOW = 125 mg, MED = 250 mg, HI = 375 mg). In experiment 2, 6 heifers (n = 3/treatment) were drenched daily for 3 d, either with 62.5 g of SS dissolved in water (SAL) or an equal volume of water (CON2). Rumen fluid was collected from each heifer and was not pooled. After the fluid was mixed 2:1 with McDougall's buffer, 150 mL of inoculum was added to the fermentation flasks (n = 4/heifer) with 2.5 g of fermentation substrate. This experiment was performed the day before SS treatment began and repeated 1, 13, and 35 d after the end of the treatment period. We also performed an in situ experiment at each of these time points. In the first experiment, inclusion of SS resulted in a decrease in dry matter disappearance (DMD) over 24 h, as well as an increase in final pH. We detected no difference between treatments for gas production asymptotic volume, rate, or lag. In the second experiment, we detected a significant treatment x day interaction for DMD: we observed no difference between groups during a 24-h batch culture on the day following treatment, but SAL resulted in lower DMD on d 13 and d 35. We detected no treatment effect on the final pH of the batch culture or on any gas-production parameters. We observed a tendency for SAL to decrease the DMD rate in situ on the day after treatment. These results indicate that SS administration has a negative effect on rumen microorganisms.

Reductions in cortical alpha activity, enhancements in neural responses and impaired gap detection caused by sodium salicylate in awake guinea pigs.[Pubmed:27862478]

Eur J Neurosci. 2017 Feb;45(3):398-409.

Tinnitus chronically affects between 10-15% of the population but, despite its prevalence, the underlying mechanisms are still not properly understood. One experimental model involves administration of high doses of Sodium salicylate, as this is known to reliably induce tinnitus in both humans and animals. Guinea pigs were implanted with chronic electrocorticography (ECoG) electrode arrays, with silver-ball electrodes placed on the dura over left and right auditory cortex. Two more electrodes were positioned over the cerebellum to monitor auditory brainstem responses (ABRs). We recorded resting-state and auditory evoked neural activity from awake animals before and 2 h following salicylate administration (350 mg/kg; i.p.). Large increases in click-evoked responses (> 100%) were evident across the whole auditory cortex, despite significant reductions in wave I ABR amplitudes (in response to 20 kHz tones), which are indicative of auditory nerve activity. In the same animals, significant decreases in 6-10 Hz spontaneous oscillations (alpha waves) were evident over dorsocaudal auditory cortex. We were also able to demonstrate for the first time that cortical evoked potentials can be inhibited by a preceding gap in background noise [gap-induced pre-pulse inhibition (PPI)], in a similar fashion to the gap-induced inhibition of the acoustic startle reflex that is used as a behavioural test for tinnitus. Furthermore, 2 h following salicylate administration, we observed significant deficits in PPI of cortical responses that were closely aligned with significant deficits in behavioural responses to the same stimuli. Together, these data are suggestive of neural correlates of tinnitus and oversensitivity to sound (hyperacusis).

Salicylic Acid and Sodium Salicylate Alleviate Cadmium Toxicity to Different Extents in Maize (Zea mays L.).[Pubmed:27490102]

PLoS One. 2016 Aug 4;11(8):e0160157.

The role of salicylic acid in Cd tolerance has attracted more attention recently but no information is available on the efficiency of different forms of salicylic acid. The aim was thus to investigate whether both the acid and salt forms of salicylic acid provide protection against Cd stress and to compare their mode of action. Young maize plants were grown under controlled environmental conditions. One group of 10-day-old seedlings were treated with 0.5 mM SA or NaSA for 1 day then half of the pants were treated with 0.5 mM Cd for 1 day. Another group of seedlings was treated with 0.5 mM CdSO4 for 1 day without pre-treatment with SA or NaSA, while a third group was treated simultaneously with Cd and either SA or NaSA. Both salicylic acid forms reduced the Cd accumulation in the roots. Treatment with the acidic form meliorated the Cd accumulation in the leaves, while Na-salicylate increased the phytochelatin level in the roots and the amount of salicylic acid in the leaves. Furthermore, increased antioxidant enzyme activity was mainly induced by the acid form, while glutathione-related redox changes were influenced mostly by the salt form. The acidic and salt forms of salicylic acid affected the two antioxidant systems in different ways, and the influence of these two forms on the distribution and detoxification of Cd also differed. The present results also draw attention to the fact that generalisations about the stress protective mechanisms induced by salicylic acid are misleading since different forms of SA may exert different effects on the plants via separate mechanisms.

Description

Sodium Salicylate inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation.

Keywords:

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