产品
编 号：F384748
分子式：C7H5NaO3
分子量：160.1
分子式：C7H5NaO3
分子量：160.1
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
500mg
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询价
10g
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50g
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结构图
CAS No: 54-21-7
产品详情
生物活性：
Sodium Salicylate (Salicylic acid sodium salt) inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation. Sodium Salicylate is also a S6K inhibitor.Sodium Salicylate is a NF-κB inhibitor that decreases inflammatory gene expression and improves repair in aged muscle.
体内研究：
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.
体外研究：
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%.
Sodium Salicylate (Salicylic acid sodium salt) inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation. Sodium Salicylate is also a S6K inhibitor.Sodium Salicylate is a NF-κB inhibitor that decreases inflammatory gene expression and improves repair in aged muscle.
体内研究：
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.
体外研究：
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%.
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