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中药性味相制配伍减毒的方法探要

ISSN号：1673-1727
期刊名称：中华中医药杂志
时间：2013.3.3
页码：595-598
分类：Q516[生物学—生物化学] TQ460.72[医药卫生—药物分析学;化学工程—制药化工]
作者机构：[1]Nanjing University of Chinese Medicine, Nanjing (210023), China, [2]Department of Rheumatology and Immunology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei (230038), China
相关基金：Supported by the National Natural Science Foundation of China （No. 81072749）, the Ministry of Education of Overseas Returnees Research Fund （No. 2006331）, Six Talent Peaks Subject of Jiangsu Province （No. 2007）, a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions （No. 20116）, Jiangsu Province Ordinary University innovative Research Project and Ordinary University innovative Research Project of Jiangsu Province （No. 2011）
相关项目：基于"异类相制"新假说的雷公藤复方配伍减毒机制研究

作者：冯哲|周学平*|

关键词：类风湿关节炎, 成纤维细胞, 细胞分化, 抑制机制, 单核细胞, 诱导性, 促分裂原活化蛋白激酶, 颗粒, Qingluo Tongbi Granule, rheumatoid arthritis, osteoclast differentiation, signaling pathway,regulation of tumor necrosis factor receptor-associated factor 6/mitogen-activated protein kinase pathways,Chinese medicine

中文摘要：

学习位于 Qingluo Tongbi 小粒的禁止的效果下面的机制，在在老鼠的风湿性关节炎的骨破折区别上的 QTG。

英文摘要：

Objective： To study the mechanism underlying the inhibitory effect of Qingluo Tongbi Granule （清络通痹颗粒, QTG） on osteoclast differentiation in rheumatoid arthritis in rats. Methods： Fibroblast and monocyte co-culture were used to induce osteoclast differentiation in adjuvant-induced arthritic （AIA） rats. Serum containing QTG was prepared and added to the osteoclasts, and activation of the tumor necrosis factor receptorassociated factor 6/mitogen-activated protein kinase/nuclear factor of activated T cells, cytoplasmic1 （TRAF6/ MAPK/NFATcl） pathways was examined. Results： The induced osteoclasts were multinucleated and stained positive for tartrate-resistant acid phosphatase （TRAP） staining. Serum containing QTG at 14.4, 7.2 or 3.6 g/kg inhibited the activation of TRAF6, extracellular regulated protein kinase （ERK）1/2, c-Jun N-terminal kinase （JNK） and p38 and decreased the percentage of cells with nuclear NFATcl in a dose-dependent manner, the high and middle doses exhibited clear inhibitory activity （P〈0.01 and P〈0.05, respectively）. After the addition of MAPK inhibitors, the NFATcl expression showed no significant difference compared with the control group （P〉0.05）. Conclusions： Serum containing QTG could generally inhibit the TRAF6/MAPK pathways and possibly inhibit the NFATcl pathway. In addition, QTG may regulate other signaling pathways that are related to osteoclast differentiation and maturation.

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