Sodium 2-Hydroxybenzoate (Sodium Salicylate) inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation[3]. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells[4]. Sodium salicylate effectively inhibited TNF-alpha-induced upregulation of NF-kappaB, ICAM-1 expression, in-vitro migration and invasion in human melanoma cells, indicating that non-steroidal anti-inflammatory drugs may be a useful therapeutic approach to oppose inflammation-induced melanoma invasion and metastasis in vivo[5]. PC12 cells were treated with different concentrations of sodium salicylate (1-20 mM). Higher concentrations (10-20 mM) killed PC12 cells in a dose-dependent manner. A decreased NF-kappaB activity after sodium salicylate treatment by electrophoretic mobility shift assay (EMSA)[6]. In the RAW264.7 macrophage cell line, suprapharmacological concentrations of sodium salicylate exert a potent inhibitory effect on LPS-induced cytokine gene induction but appear to accomplish this by interfering with NF-kappaB-independent pathways of activation[7]. Moreover, salicylate significantly improved retinal function, as well as reduced TNFα and SOCS3-induced insulin resistance in all samples[8].
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