Abstract
The N-salicyloyltryptamine (NST) is an indole derivative compound analogue to the alkaloid N-benzoyltryptamine. In the present study, the antiedematogenic activity of NST was investigated in animal models. Firstly, the acute toxicity for NST was assessed according to the OECD Guideline no. 423. The potential NST-induced antiedematogenic activity was evaluated by carrageenan-induced paw edema in rats, as well as by dextran-, compound 48/80-, histamine-, serotonin-, capsaicine-, and prostaglandin E2-induced paw edema in mice. The effect of NST on compound 48/80-induced ex vivo mast cell degranulation on mice mesenteric bed was investigated. No death or alteration of behavioral parameters was observed after administration of NST (2000 mg/kg, i.p.) during the observation time of 14 days. The NST (100 and 200 mg/kg, i.p.) inhibited the carrageenan-induced edema from the 1st to the 5th hour (**p<0.01; ***p<0.001). The edematogenic activity induced by dextran, compound 48/80, histamine, serotonin, capsaicin, and prostaglandin E2 was inhibited by NST (100 mg/kg, i.p.) throughout the observation period (**p<0.01; ***p<0.001). The pretreatment with NST (50, 100 or 200 mg/kg, i.p) attenuates the compound 48/80-induced mast cell degranulation (**p<0.01; ***p<0.001). Thus, the inhibition of both mast cell degranulation and release of endogenous mediators are probably involved in the NST-induced antiedematogenic effect.
Highlights
Inflammation involves the participation of a wide sort of biological mediators, such as histamine, serotonin, bradykinin, and prostaglandins
The chemical structure of NST consists of an indole core related to the N-benzoyltryptamine, an indole alkaloid isolated from Myrtopsis myrtoidea (Baill) Guillaumin (Hifnawy 1957)
Reported that several indole derivative compounds are able to promote anti-inflammatory activities in different experimental models of paw edema induced by carrageenan, dextran, and histamine (Barbosa-Filho et al 2006)
Summary
Inflammation involves the participation of a wide sort of biological mediators, such as histamine, serotonin, bradykinin, and prostaglandins. These inflammatory agents promote vasodilation and neutrophil migration from blood towards inflamed tissues (Hajare et al 2001). The lack of the recovery of the injured area increases the damage by formation of granulation tissue and accumulation of secretory cells (enzymes and free radicals), which positively increases the local inflammation, impairing the repair of damaged area (Dinarello 2010). The drugs commonly used in the treatment of inflammation include the non-steroidal and steroidal anti-inflammatory drugs, which are able to promote several side effects, such as gastric ulcers, dyspepsia, bleeding and cardiovascular disorders (Dinarello 2010, Narum et al 2014). The discovery of new drugs for the treatment of inflammatory diseases which present good therapeutic efficacy and fewer side effects is strongly necessary
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