IR@PKUHSC  > 北京大学药学院
学科主题药学
Antinociception of spirocyclopiperazinium salt compound LXM-10-M targeting alpha 7 nicotinic receptor and M4 muscarinic receptor and inhibiting CaMKII alpha/CREB/CGRP signaling pathway in mice
Wan, Dan1; Wang, Ding1; Sun, Qi2; Song, Yan1; Jiang, YiMin3; Li, RunTao2; Ye, Jia1
关键词Spirocyclopiperazinium Salt Compound Lxm-10-m Antinociception Alpha 7 Nicotinic Receptor M4 Muscarinic Receptor Camkii Alpha/creb/cgrp Signaling Pathway
刊名EUROPEAN JOURNAL OF PHARMACOLOGY
2016-01-05
DOI10.1016/j.ejphar.2015.11.056
770页:92-98
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy
研究领域[WOS]Pharmacology & Pharmacy
关键词[WOS]DEPENDENT PROTEIN-KINASE ; ELEMENT-BINDING PROTEIN ; GENE-RELATED PEPTIDE ; INFLAMMATORY PAIN ; RATS ; MODELS ; PHOSPHORYLATION ; ACTIVATION ; BEHAVIOR ; NUCLEUS
英文摘要

The present study was designed to investigate the antinociception of spirocyclopiperazinium salt compound LXM-10-M (2,4-dimethyl-9-beta m-hydroxyphenylethyl-3-oxo-6, 9-diazaspiro [5.5] undecane chloride) in thermal and chemical pain models, and further to explore the molecular target and potential signal pathway. We assessed the antinociception of LXM-10-M in hot-plate test, formalin test and acetic acid writhing test in mice. The possible changes of calcium/calmodulin-dependent protein kinase II alpha (CaMKII alpha)/cAMP response element-binding protein (CREB)/calcitonin gene related peptide (CGRP) signaling pathway were detected by Western Blot in mice. Administration of LXM-10-M produced significant antinociception in hot-plate test, formalin test and acetic acid writhing test in mice, with no obvious toxicity. The antinociceptive effects were blocked by pretreatment with methyllycaconitine citrate (MLA, alpha 7 nicotinic receptor antagonist) or tropicamide (TRO, M4 muscarinic receptor antagonist). Western blot analysis showed that the upregulations of p-CaMKII alpha, p-CREB and CGRP in the spinal cord were reduced by LXM-10-M in chemical pain model in mice, and the effects were blocked by MLA or TRO pretreatment. This is the first paper to report that LXM-10-M exerted significant antinociception, which may be attributed to the activation of alpha 7 nicotinic receptor and M4 muscarinic receptor and thereby triggering the inhibition of CaMKII alpha/CREB/CGRP signaling pathway in mice. (C)) 2015 Elsevier By. All rights reserved.

语种英语
WOS记录号WOS:000367230700013
项目编号81470050 ; 7122097
资助机构National Natural Science Foundation of China, China ; Beijing Municipal Natural Science Foundation, China
引用统计
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56792
专题北京大学药学院
北京大学医学部管理机构_医学部
北京大学药学院_化学生物学系
北京大学药学院_分子与细胞药理学系
作者单位1.Peking Univ, Sch Pharmaceut Sci, Dept Mol & Cellular Pharmacol, Beijing 100871, Peoples R China
2.Peking Univ, Sch Pharmaceut Sci, Dept Biol Chem, Beijing 100871, Peoples R China
3.Peking Univ, Med & Hlth Anal Ctr, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Wan, Dan,Wang, Ding,Sun, Qi,et al. Antinociception of spirocyclopiperazinium salt compound LXM-10-M targeting alpha 7 nicotinic receptor and M4 muscarinic receptor and inhibiting CaMKII alpha/CREB/CGRP signaling pathway in mice[J]. EUROPEAN JOURNAL OF PHARMACOLOGY,2016,770:92-98.
APA Wan, Dan.,Wang, Ding.,Sun, Qi.,Song, Yan.,Jiang, YiMin.,...&Ye, Jia.(2016).Antinociception of spirocyclopiperazinium salt compound LXM-10-M targeting alpha 7 nicotinic receptor and M4 muscarinic receptor and inhibiting CaMKII alpha/CREB/CGRP signaling pathway in mice.EUROPEAN JOURNAL OF PHARMACOLOGY,770,92-98.
MLA Wan, Dan,et al."Antinociception of spirocyclopiperazinium salt compound LXM-10-M targeting alpha 7 nicotinic receptor and M4 muscarinic receptor and inhibiting CaMKII alpha/CREB/CGRP signaling pathway in mice".EUROPEAN JOURNAL OF PHARMACOLOGY 770(2016):92-98.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Wan, Dan]的文章
[Wang, Ding]的文章
[Sun, Qi]的文章
百度学术
百度学术中相似的文章
[Wan, Dan]的文章
[Wang, Ding]的文章
[Sun, Qi]的文章
必应学术
必应学术中相似的文章
[Wan, Dan]的文章
[Wang, Ding]的文章
[Sun, Qi]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。