Abstract
Nitric oxide (NO) has been proposed to play a role in a variety of inflammatory diseases. Sodium salicylate (NaSal) is the most commonly used anti-inflammatory agent. We investigated whether NaSal can diminish the production of NO in TM4 Sertoli cells. TM4 Sertoli cells produced a small amount of NO upon treatment with recombinant interferon-γ (rIFN-γ). The effect of rIFN-γ was enhanced markedly by the addition of recombinant TNF-α (rTNF-α) in a dose-dependent manner. NaSal (10 and 20 mM) significantly inhibited NO production from TM4 Sertoli cells induced by rIFN-γ plus rTNF-α. In addition, rIFN-γ in combination with rTNF-α showed a marked increase of the expression of inducible NO synthase (iNOS) protein. Western blot analysis revealed that NaSal (10 and 20 mM) blocked a step of iNOS protein synthesis. The rIFN-γ plus rTNF-α-induced nuclear factor-κB (NF-κB) activation was significantly blocked by NaSal (10 and 20 mM). On the other hand, neither staurosporine nor polymyxin B significantly inhibited NO production from TM4 Sertoli cells induced by rIFN-γ plus rTNF-α. The present results indicate that NaSal inhibits rIFN-γ plus rTNF-α-induced NO production in TM4 Sertoli cells via the signal transduction pathway of NF-κB activation.
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