Salicylic acid (2-Hydroxybenzoic acid) inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation^[1].

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 E₂release when add together with interleukin 1β for 24 hr with an IC₅₀value 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 IC₅₀of >100 μg/mL. When added together with IL-1β for 24 hr, Salicylic acid causes a concentration-dependent inhibition of PGE₂release with an apparent IC₅₀value 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 IC₅₀value 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 IC₅₀value 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].

138.12

Solid

C₇H₆O₃

69-72-7

水杨酸

• Phenols
• Monophenols

• Ketones, Aldehydes, Acids

• Plants
• other families

Room temperature in continental US; may vary elsewhere.

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

DMSO : ≥ 50 mg/mL(362.00 mM)

H₂O : 1 mg/mL(7.24 mM;Need ultrasonic)

*"≥" means soluble, but saturation unknown.

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℃, 6 months; -20℃, 1 month (protect from light)。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 2.5 mg/mL (18.10 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (18.10 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 2.

  请依序添加每种溶剂： 10% DMSO    90% (20%SBE-β-CDin saline)

  Solubility: 2.5 mg/mL (18.10 mM); Clear solution; Need ultrasonic

  此方案可获得 2.5 mg/mL (18.10 mM) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: 2.5 mg/mL (18.10 mM); Clear solution; Need ultrasonic

  此方案可获得 2.5 mg/mL (18.10 mM) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。