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
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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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