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大麻素受体1的拮抗作用减弱了电针在偏头痛啮齿动物模型中的抗炎作用。

Antagonism of cannabinoid receptor 1 attenuates the anti-inflammatory effects of electroacupuncture in a rodent model of migraine.

作者信息

Zhang Hui, He Shengdong, Hu Youping, Zheng Hui

机构信息

Department of Acupuncture and Moxibustion, School of Traditional Chinese Medicine Combined with Western Medicine, Southwest Medical University, Luzhou, Sichuan, China.

Department of Respirology, The affiliated Hospital, Southwest Medical University, Luzhou, Sichuan, China.

出版信息

Acupunct Med. 2016 Dec;34(6):463-470. doi: 10.1136/acupmed-2016-011113. Epub 2016 Nov 10.

Abstract

BACKGROUND

The anti-nociceptive effects of electroacupuncture (EA) in migraine have been documented in multiple randomised controlled trials. Neurogenic inflammation plays a key role in migraine attacks, and the anti-inflammatory effects of acupuncture have been associated with the type 1 cannabinoid (CB1) receptor.

OBJECTIVE

To investigate whether CB1 receptors mediate the anti-inflammatory effects of EA on migraine attacks.

METHODS

A migraine model was produced in Sprague-Dawley rats by unilateral electrical stimulation of the trigeminal ganglion (TGES). Rats received EA daily on the 5 days preceding TGES with (TGES+EA+SR141716 group) or without (TGES+EA group) intraperitoneal injections of the CB1 receptor antagonist SR141716. Another group of TGES rats (TGES+MA group) and a non-TGES sham-operated group of rats (Sham+MA group) received minimal acupuncture (MA). Calcitonin gene-related peptide (CGRP) and prostaglandin E2 (PGE2) concentrations were determined in serum obtained from the ipsilateral jugular vein at initiation of TGES and 5 min after. Postmortem interleukin (IL)-1β and cyclooxygenase (COX)2 protein levels in the trigeminal ganglion (TG) and plasma protein extravasation (PPE) in the dura mater were assessed.

RESULTS

TGES induced increases in serum CGRP and PGE2 levels (TGES+MA vs baseline and vs Sham: all p<0.001), as well as IL-1β and COX2 protein expression in the TG, and neurogenic PPE levels (TGES+MA vs Sham+MA: all p<0.001). EA attenuated TGES-induced increases in the levels of these proteins (TGES+EA vs TGES+MA: all p<0.001). CB1 receptor antagonism reversed the effects of EA (TGES+EA+SR141716 vs TGES+EA: all p<0.05).

CONCLUSIONS

CB1 receptors appear to mediate anti-inflammatory effects of EA in a rat model of migraine.

摘要

背景

多项随机对照试验已证明电针(EA)对偏头痛具有抗伤害感受作用。神经源性炎症在偏头痛发作中起关键作用,且针刺的抗炎作用与1型大麻素(CB1)受体有关。

目的

研究CB1受体是否介导EA对偏头痛发作的抗炎作用。

方法

通过单侧电刺激三叉神经节(TGES)在Sprague-Dawley大鼠中建立偏头痛模型。在TGES前5天,大鼠每天接受EA治疗,其中一组(TGES+EA+SR141716组)腹腔注射CB1受体拮抗剂SR141716,另一组(TGES+EA组)不注射。另一组TGES大鼠(TGES+MA组)和一组非TGES假手术大鼠(Sham+MA组)接受微量针刺(MA)。在TGES开始时和5分钟后,从同侧颈静脉采集血清,测定降钙素基因相关肽(CGRP)和前列腺素E2(PGE2)浓度。评估三叉神经节(TG)中的死后白细胞介素(IL)-1β和环氧化酶(COX)2蛋白水平以及硬脑膜中的血浆蛋白外渗(PPE)。

结果

TGES导致血清CGRP和PGE2水平升高(TGES+MA组与基线和假手术组相比:所有p<0.001),以及TG中IL-1β和COX2蛋白表达和神经源性PPE水平升高(TGES+MA组与Sham+MA组相比:所有p<0.001)。EA减轻了TGES诱导的这些蛋白水平升高(TGES+EA组与TGES+MA组相比:所有p<0.001)。CB1受体拮抗作用逆转了EA的作用(TGES+EA+SR141716组与TGES+EA组相比:所有p<0.05)。

结论

在偏头痛大鼠模型中,CB1受体似乎介导了EA的抗炎作用。

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