中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Studies on the mechanism underlying the inhibition of RANKL-induced differentiation of RAW264.7 cells into osteoclasts by sulfated amylopectin

文献类型:期刊论文

作者Chen Cheng1; Fang Jianping2; Wang Ying2; Wang Haiying1; Ding Kan2
刊名Chinese Journal New Drugs
出版日期2014
卷号23期号:1页码:25-31
关键词IkappaBalpha ERK sulfated amylopectin nuclear factor kappa B ligand osteoclast IkappaBalpha ERK
ISSN号1003-3734
其他题名硫酸化支链淀粉抑制RANKL诱导破骨细胞的形成及其作用机制
文献子类Article
英文摘要Objective: To prepare sulfated amylopectin (SA) and study its effect and underlying molecular mechanism for the receptor activator of nuclear factor kappa B ligand (RANKL)-induced differentiation of RAW264.7 macrophages into osteoclasts. Methods: SA was synthesized by chlorosulfonic acid-pyridine method. The sulfation position and substitution degree of SA were determined with infrared spectrascopy, ~(13)C-NMR spectra, and Barium chloride-alum turbidimetric method, respectively. The cytotoxicity of SA on RAW264.7 cells was evaluated using MTT assay. To study the effect of SA on RANKL-induced differentiation of RAW264.7 macrophages into osteoclasts, the tartrate resistant acid phosphatase (TRAP) staining assay was used to observe the morphology of osteoclasts, and RT-PCR was employed to determine the expression levels of marker genes in osteoclasts such as TRAP and Cathepsin K. Moreover, immunoblotting was used to investigate the influence of SA on the RANKL activated signaling such as ERK and NF-kappaB. Results: Sulfated amylopectin was prepared with the major sulfation position at C-6, and its degree of sulfation was 1.07. When the concentration was less than or equal to 20 mug·mL~(-1), SA had no significant effect on the cell proliferation. SA could inhibit RANKL-induced differention of RAW26.7 cells into osteoclasts. RANKL-induced phosphorylation of ERK and degradation of IkappaBalpha were impaired when RAW264.7 cells were treated with SA. Conclusion: The synthesized sulfated amylopectin could block RANKL-induced differentiation of RAW264.7 cells into osteoclasts via inhibition of activation of ERK and NF-kappaB signaling partially.
资助项目国家"重大新药创制"科技重大专项[00000000]
WOS研究方向Pharmacology & Pharmacy (provided by Clarivate Analytics)
语种中文
CSCD记录号CSCD:5038809
源URL[http://119.78.100.183/handle/2S10ELR8/269354]  
专题药理学第三研究室
通讯作者Ding Kan
作者单位1.Institute of Traditional Chinese Medicine, Shanghai Tradional Chinese Medicine University, Shanghai 201203, China.;
2.Glycochemistry and Glycobiology Laboratory, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
推荐引用方式
GB/T 7714
Chen Cheng,Fang Jianping,Wang Ying,et al. Studies on the mechanism underlying the inhibition of RANKL-induced differentiation of RAW264.7 cells into osteoclasts by sulfated amylopectin[J]. Chinese Journal New Drugs,2014,23(1):25-31.
APA Chen Cheng,Fang Jianping,Wang Ying,Wang Haiying,&Ding Kan.(2014).Studies on the mechanism underlying the inhibition of RANKL-induced differentiation of RAW264.7 cells into osteoclasts by sulfated amylopectin.Chinese Journal New Drugs,23(1),25-31.
MLA Chen Cheng,et al."Studies on the mechanism underlying the inhibition of RANKL-induced differentiation of RAW264.7 cells into osteoclasts by sulfated amylopectin".Chinese Journal New Drugs 23.1(2014):25-31.

入库方式: OAI收割

来源:上海药物研究所

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