Salicylic acid
(Synonyms: 水杨酸; 2-Hydroxybenzoic acid) 目录号 : GC16508
An Analytical Reference Standard
Cas No.:69-72-7
Sample solution is provided at 25 µL, 10mM.
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Salicylic acid inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation.
Salicylic acid is an effective inhibitor of COX-2 activity at concentrations far below those required to inhibit NF-κB (20 mg/mL) activation. Salicylic acid 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. Salicylic acid 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, Salicylic acid 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, Salicylic acid causes a concentration-dependent inhibition of PGE2 release with an apparent IC50 value of approximately 5 μg/mL. The ability of Salicylic acid 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). Salicylic acid 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, Salicylic acid 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 C57Bl/6 DIO mice, Salicylic acid decreases both fasting and postprandial plasma glucose levels. Furthermore, there is a trend to reduce plasma triglyceride levels after Salicylic acid treatment in C57Bl/6 DIO mice (P=0.059). Salicylic acid 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, Salicylic acid 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.
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Kinase experiment: |
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 Salicylic acid 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]. |
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Cell experiment: |
To assess the direct effect of Salicylic acid 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 Salicylic acid(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]. |
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Animal experiment: |
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. Salicylic acid (120 mg/kg/day) 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. |
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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. |
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| Cas No. | 69-72-7 | SDF | |
| 别名 | 水杨酸; 2-Hydroxybenzoic acid | ||
| 化学名 | 2-hydroxybenzoic acid | ||
| Canonical SMILES | C1=CC=C(C(=C1)C(=O)O)O | ||
| 分子式 | C7H6O3 | 分子量 | 138.12 |
| 溶解度 | ≥ 6.9mg/mL in DMSO | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 7.2401 mL | 36.2004 mL | 72.4008 mL |
| 5 mM | 1.448 mL | 7.2401 mL | 14.4802 mL |
| 10 mM | 0.724 mL | 3.62 mL | 7.2401 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet