Objective and design

The involvement of nitric oxide pathway in the antinociceptive activity of Lonchocarpus araripensis lectin (LAL) was investigated in the model of carragenan-induced hypernociception.

Methods

Swiss mice received LAL (0.01–10 mg/kg; i.v.) 30 min before s.c. injection of carragenan in the paws. For the involvement of nociceptive pathways, animals were previously treated with the blockers: NOS (L-NAME, aminoguanidine, 7-nitroindazole); soluble guanylyl cyclase (ODQ); channels of ATP-dependent K⁺ (glibenclamide); L-type Ca²⁺ (nifedipine), or Ca²⁺-dependent Cl⁻ (niflumic acid). Participation of lectin domain was evaluated by injection of LAL associated with N-acetyl-glucosamine (GlcNAc). nNOS gene relative expression was evaluated in the paw tissues and nNOS immunostaining in dorsal root ganglia.

Results

LAL at all doses inhibited carrageenan-induced hypernociception (4.12 ± 0.58 g), being maximal at 10 mg/kg (3 h: 59%), and reversed by GlcNAc. At this time, LAL effect was reversed by nifedipine (39%), niflumic acid (59%), L-NAME (59%), 7-nitroindazole (44%), ODQ (45%), and glibenclamide (34%), but was unaltered by aminoguanidine. LAL increased (95%) nNOS gene expression in mice paw tissues, but not its immunoexpression in the dorsal root ganglia.

Conclusion

The antinociceptive effect of Lonchocarpus araripensis lectin involves activation of the l-arginine/NO/GMPc/K⁺ATP pathway.

中文翻译：

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阿拉伯扁果凝集素的镇痛作用：激活L-精氨酸/ NO / cGMP / K + ATP信号通路。

目标和设计

一氧化氮途径的的镇痛活性的参与薄荚豆属araripensis凝集素（LAL）在角叉菜胶诱导的超伤害的模型进行了研究。

方法

瑞士小鼠在皮下注射角叉菜胶前30分钟接受LAL（0.01-10 mg / kg; iv）。由于涉及伤害感受途径，因此预先用阻断剂治疗动物：NOS（L-NAME，氨基胍，7-硝基吲唑）；可溶性鸟苷酸环化酶（ODQ）；ATP依赖性K ⁺（格列本脲）通道；L-型Ca ²⁺（硝苯地平），或Ca ²⁺依赖性氯^- （尼氟酸）。凝集素结构域的参与通过注射与N-乙酰氨基葡萄糖（GlcNAc）相关的LAL进行评估。评估爪组织中nNOS基因的相对表达以及背根神经节中nNOS的免疫染色。

结果

所有剂量的LAL均抑制角叉菜胶诱导的痛觉过敏（4.12±0.58 g），最大剂量为10 mg / kg（3 h：59％），并被GlcNAc逆转。此时，硝苯地平（39％），尼氟酸（59％），L-NAME（59％），7-硝基吲唑（44％），ODQ（45％）和格列本脲（34％）逆转了LAL的作用。 ，但未被氨基胍改变。LAL增加了小鼠爪组织中nNOS基因的表达（95％），但在背根神经节中没有免疫表达。

结论

的镇痛效果薄荚豆属araripensis凝集素涉及的激活升精氨酸/ NO / GMPC / K ⁺ ATP通路。