α-双abolol对小鼠内脏痛觉的抑制作用:机制探讨。

Gerlânia de Oliveira Leite, Cícera Norma Fernandes, Irwin Rose Alencar de Menezes, José Galberto Martins da Costa, Adriana Rolim Campos
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引用次数: 24

摘要

背景:我们之前在环磷酰胺和芥菜油(MO)诱导的内脏伤害性小鼠模型中描述了α-双abolol (BISA)的内脏抗伤害性。本研究考察了BISA在醋酸、辣椒素、福尔马林诱导的内脏伤害性小鼠模型中的作用,以及一氧化氮系统、α2、KATP、5-HT3和TRPV1受体在BISA对mo诱发的伤害性行为的影响中的作用。小鼠分别口服BISA(50、100和200 mg/kg)或对照物,分析腹腔注射乙酸或结肠内注射MO对小鼠疼痛相关行为的影响。结果:BISA对伤害性行为的抑制作用呈剂量无关。BISA (50 mg/kg)对格列本脲具有耐药作用,但未被其他拮抗剂预处理阻断。在检测镇静或运动异常的开场试验中,50mg /kg BISA对小鼠的行走频率没有任何影响。结论:然而,它们的确切抗感觉作用机制尚未确定。
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Attenuation of visceral nociception by α-bisabolol in mice: investigation of mechanisms.

Background: We previously described the visceral antinociceptive property of α-bisabolol (BISA) in mouse models of visceral nociception induced by cyclophosphamide and mustard oil (MO). This study examined the effect of BISA in mouse models of visceral nociception induced by acetic acid, capsaicin, formalin, and the contribution of the nitric oxide system, α2, KATP, 5-HT3 and TRPV1 receptors to the effect of BISA on MO-evoked nociceptive behaviors. Mice were pretreated orally with BISA (50, 100 and 200 mg/kg) or vehicle, and the pain-related behavioral responses to intraperitoneal administration of acetic acid or intracolonic injection of MO were analyzed.

Results: BISA significantly suppressed the nociceptive behaviors in a dose-unrelated manner. The antinociceptive effect of BISA (50 mg/kg) was show to be glibenclamide resistant, but it was not blocked by pretreatment with the other antagonists tested. In the open-field test that detects sedative or motor abnormality, mice received 50 mg/kg BISA did not show any per se influence in ambulation frequency.

Conclusions: However, their precise antinociceptive mechanisms of action have not been determined.

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