α-红没药醇对小鼠内脏痛觉的减轻作用：作用机制研究
Attenuation of visceral nociception by α-bisabolol in mice: investigation of mechanisms.
作者信息
Leite Gerlânia de Oliveira, Fernandes Cícera Norma, de Menezes Irwin Rose Alencar, da Costa José Galberto Martins, Campos Adriana Rolim
机构信息
Vice-Reitoria de Pesquisa e Pós-Graduação, Universidade de Fortaleza, Av, Washington Soares, 1321, Fortaleza, Ceará, CEP 60811-905, Brazil.
出版信息
Org Med Chem Lett. 2012 May 21;2(1):18. doi: 10.1186/2191-2858-2-18.
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.
背景
我们之前在环磷酰胺和芥子油（MO）诱导的内脏痛觉过敏小鼠模型中描述了α-红没药醇（BISA）的内脏抗伤害感受特性。本研究检测了BISA在乙酸、辣椒素、福尔马林诱导的内脏痛觉过敏小鼠模型中的作用，以及一氧化氮系统、α2、KATP、5-HT3和TRPV1受体对BISA对MO诱发的伤害性行为作用的贡献。小鼠口服BISA（50、100和200mg/kg）或赋形剂进行预处理，分析腹腔注射乙酸或结肠内注射MO后与疼痛相关的行为反应。
结果
BISA以剂量无关的方式显著抑制伤害性行为。BISA（50mg/kg）的抗伤害感受作用显示对格列本脲耐药，但未被所测试的其他拮抗剂预处理所阻断。在检测镇静或运动异常的旷场试验中，接受50mg/kg BISA的小鼠在行走频率上未表现出任何自身影响。
结论
然而，其确切的抗伤害感受作用机制尚未确定。
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