Sodium salicylate-induced amelioration of experimental autoimmune encephalomyelitis in Lewis rats is associated with the suppression of inducible nitric oxide synthase and cyclooxygenases.
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Moon C, Ahn M, Jee Y, Heo S, Kim S, Kim H, Sim KB, Koh CS, Shin YG, Shin T
Sodium salicylate-induced amelioration of experimental autoimmune encephalomyelitis in Lewis rats is associated with the suppression of inducible nitric oxide synthase and cyclooxygenases.
Neurosci Lett. 2004 Feb 12;356(2):123-6.
- PubMed ID
- 14746879 [ View in PubMed]
- Abstract
We studied the effects of oral administration of sodium salicylate on the expression of the pro-inflammatory mediators, nitric oxide synthase (iNOS) and cyclooxygenase- (COX-) 1 and 2, in rats with experimental autoimmune encephalomyelitis (EAE). Sodium salicylate (200 mg/kg) was administered orally for 13 days after the induction of EAE by immunization with guinea pig myelin basic protein and complete Freund's adjuvant. The onset (P<0.0001) and severity (P<0.05) of EAE paralysis in salicylate-treated animals were delayed and suppressed significantly compared with vehicle-treated controls. Western blot analysis showed that expression of COX-2 and iNOS, but not COX-1, decreased significantly in the spinal cords of salicylate-treated rats compared with vehicle-treated controls (P<0.05) and this finding was paralleled by immunohistochemical observations. These results suggest that the amelioration by salicylate of paralysis in rats with EAE is mediated in part by the suppression of COX and iNOS.
DrugBank Data that Cites this Article
- Drug Targets
Drug Target Kind Organism Pharmacological Action Actions Magnesium salicylate Prostaglandin G/H synthase 1 Protein Humans YesInhibitorDetails Salicylic acid Prostaglandin G/H synthase 1 Protein Humans YesInhibitorDetails