Sousa-Neto Benedito P, Gomes Bruno S, Cunha Francisco V M, Arcanjo Daniel D R, Gutierrez Stanley J C, Souza Maria F V, Almeida Fernanda R C, Oliveira Francisco A
Núcleo de Pesquisas em Plantas Medicinais, Universidade Federal do Piauí, Av. Universitária, s/n, Campus Ministro Petrônio Portella, SG-15, Ininga, 64049-550 Teresina, PI, Brazil.
Departamento de Biofísica e Fisiologia, Universidade Federal do Piauí, Av. Universitária, s/n, Campus Ministro Petrônio Portella, SG-08/09, Ininga, 64049-550 Teresina, PI, Brazil.
An Acad Bras Cienc. 2018 Jan-Mar;90(1):185-194. doi: 10.1590/0001-3765201720160502.
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.
N-水杨酰色胺（NST）是一种与生物碱N-苯甲酰色胺类似的吲哚衍生物化合物。在本研究中，在动物模型中研究了NST的抗水肿活性。首先，根据经合组织第423号指南评估NST的急性毒性。通过角叉菜胶诱导的大鼠爪肿胀以及葡聚糖、化合物48/80、组胺、5-羟色胺、辣椒素和前列腺素E2诱导的小鼠爪肿胀来评估NST潜在的抗水肿活性。研究了NST对化合物48/80诱导的小鼠肠系膜床离体肥大细胞脱颗粒的影响。在14天的观察期内，腹腔注射NST（2000mg/kg）后未观察到死亡或行为参数改变。NST（100和200mg/kg，腹腔注射）在第1至5小时抑制了角叉菜胶诱导的肿胀（**p<0.01；***p<0.001）。在整个观察期内，NST（100mg/kg，腹腔注射）抑制了葡聚糖、化合物48/80、组胺、5-羟色胺、辣椒素和前列腺素E2诱导的致肿活性（**p<0.01；***p<0.001）。用NST（50、100或200mg/kg，腹腔注射）预处理可减轻化合物48/80诱导的肥大细胞脱颗粒（**p<0.01；***p<0.001）。因此，肥大细胞脱颗粒的抑制和内源性介质的释放可能都参与了NST诱导的抗水肿作用。
