Sodium salicylate

Research use only, not for human use.

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

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

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%.

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.

Sodium salicylate | Kerasalicyl | Kerosal | Magsalyl

Chromatin/Epigenetic

COX

COX-1| COX-3| NF-κB

Inflammation/Immunology

——

54-21-7

160.11

C7H5NaO3

>98% (HPLC)

Water: 32 mg/mL (198.62 mM); DMSO: 32 mg/mL (198.62 mM)

O=C([O-])C1=CC=CC=C1O.[Na+]

Benzoic acid, 2-hydroxy-, monosodium salt

(-20℃)

With Ice Pack

≥ 2 years