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小鼠口服 decursinol 的抗伤害感受机制。

Antinociceptive mechanisms of orally administered decursinol in the mouse.

作者信息

Choi Seong-Soo, Han Ki-Jung, Lee Jin-Koo, Lee Han-Kyu, Han Eun-Jung, Kim Do-Hoon, Suh Hong-Won

机构信息

Department of Pharmacology, College of Medicine, and Institute of Natural Medicine, Hallym University, 1 Okchun-dong, Chunchon, Kangwon Do, 200-702, South Korea.

出版信息

Life Sci. 2003 Jun 13;73(4):471-85. doi: 10.1016/s0024-3205(03)00311-4.

DOI:10.1016/s0024-3205(03)00311-4
PMID:12759141
Abstract

Antinociceptive profiles of decursinol were examined in ICR mice. Decursinol administered orally (from 5 to 200 mg/kg) showed an antinociceptive effect in a dose-dependent manner as measured by the tail-flick and hot-plate tests. In addition, decursinol attenuated dose-dependently the writhing numbers in the acetic acid-induced writhing test. Moreover, the cumulative response time of nociceptive behaviors induced by an intraplantar formalin injection was reduced by decursinol treatment during the both 1st and 2nd phases in a dose-dependent manner. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of TNF-alpha (100 pg), IL-1 beta (100 pg), IFN-gamma (100 pg), substance P (0.7 microg) or glutamate (20 microg) was dose-dependently diminished by decursinol. Intraperitoneal (i.p.) pretreatment with yohimbine, methysergide, cyproheptadine, ranitidine, or 3,7-dimethyl-1-propargylxanthine (DMPX) attenuated inhibition of the tail-flick response induced by decursinol. However, naloxone, thioperamide, or 1,3-dipropyl-8-(2-amino-4-chloro-phenyl)-xanthine (PACPX) did not affect inhibition of the tail-flick response induced by decursinol. Our results suggests that decursinol shows an antinociceptive property in various pain models. Furthermore, antinociception of decursinol may be mediated by noradrenergic, serotonergic, adenosine A(2), histamine H(1) and H(2) receptors.

摘要

在ICR小鼠中检测了紫花前胡醇的抗伤害感受特性。口服给予紫花前胡醇(5至200毫克/千克),通过甩尾试验和热板试验测量,其呈现出剂量依赖性的抗伤害感受作用。此外,在醋酸诱导扭体试验中,紫花前胡醇能剂量依赖性地减少扭体次数。而且,在福尔马林足底注射诱导的伤害性行为的两个阶段中,紫花前胡醇处理均能剂量依赖性地减少累积反应时间。此外,鞘内注射肿瘤坏死因子-α(100皮克)、白细胞介素-1β(100皮克)、干扰素-γ(100皮克)、P物质(0.7微克)或谷氨酸(20微克)后,紫花前胡醇能剂量依赖性地减少累积伤害性反应时间。用育亨宾、甲基麦角新碱、赛庚啶、雷尼替丁或3,7-二甲基-1-炔丙基黄嘌呤(DMPX)进行腹腔预处理,可减弱紫花前胡醇诱导的甩尾反应抑制作用。然而,纳洛酮、硫代哌啶或1,3-二丙基-8-(2-氨基-4-氯苯基)-黄嘌呤(PACPX)并不影响紫花前胡醇诱导的甩尾反应抑制作用。我们的结果表明,紫花前胡醇在多种疼痛模型中表现出抗伤害感受特性。此外,紫花前胡醇的抗伤害感受作用可能由去甲肾上腺素能、5-羟色胺能、腺苷A(2)、组胺H(1)和H(2)受体介导。

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