Down-regulation of NR2B receptors partially contributes to analgesic effects of Gentiopicroside in persistent inflammatory pain
Down-regulation of NR2B receptors partially contributes to analgesic effects of Gentiopicroside in persistent inflammatory pain
复制标题
NR2B 受体的下调部分促进了龙胆苦苷对持续性炎性疼痛的镇痛作用
DOI：
10.1016/j.neuropharm.2008.03.007
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发表时间：
2008-06-01
影响因子：
4.7
通讯作者：
Zhao, Ming-Gao
中科院分区：
文献类型：
--
作者：
Chen, Lei;Liu, Jin-cheng;Zhao, Ming-Gao
龙胆苦苷是从黄龙胆中分离出的一种裂环烯醚萜类化合物。它在小鼠中表现出镇痛活性。前扣带皮层（ACC）是一种前脑结构，因其在疼痛传递和调节中的作用而闻名。疼痛刺激增强前额叶突触传递并诱导ACC中谷氨酸NMDA NR2B受体表达。但关于龙胆苦苷对持续性炎性疼痛以及ACC中慢性疼痛诱导的突触传递变化知之甚少。本研究旨在探讨其对周围疼痛性炎症的镇痛活性和中枢突触调节作用。龙胆苦苷对小鼠的持续性炎性疼痛刺激产生显著的镇痛作用。在小鼠后爪给予完全弗氏佐剂（CFA）引起持续性炎症的慢性阶段，全身给予龙胆苦苷显著逆转了NR2B的过度表达。全细胞膜片钳记录显示，龙胆苦苷显著降低了ACC中NR2B受体介导的突触后电流。我们的研究结果提供了有力证据，表明龙胆苦苷的镇痛作用涉及下调ACC中对持续性炎性疼痛的NR2B受体。（c）2008爱思唯尔有限公司。保留所有权利。
Gentiopicroside is one of the secoiridoid compound isolated from Gentiana lutea. It exhibits analgesic activities in the mice. The anterior cingulate cortex (ACC) is a forebrain structure known for its roles in pain transmission and modulation. Painful stimuli potentiate the prefrontal synaptic transmission and induce glutamate NMDA NR2B receptor expression in the ACC. But little is known about Gentiopicroside on the persistent inflammatory pain and chronic pain-induced synaptic transmission changes in the ACC. The present study was undertaken to investigate its analgesic activities and central synaptic modulation to the peripheral painful inflammation. Gentiopicroside produced significant analgesic effects against persistent inflammatory pain stimuli in mice. Systemic administration of Gentiopicroside significantly reversed NR2B over-expression during the chronic phases of persistent inflammation caused by hind-paw administration of complete Freunds adjuvant (CFA) in mice. Whole-cell patch clamp recordings revealed that Gentiopicroside significantly reduced NR2B receptors mediated postsynaptic currents in the ACC. Our findings provide strong evidence that analgesic effects of Gentiopicroside involve down-regulation of NR2B receptors in the ACC to persistent inflammatory pain. (c) 2008 Elsevier Ltd. All rights reserved.