CDr10b inhibits the expression of cyclooxygenase-2 and inducible nitric oxide synthase induced by lipopolysaccharide

被引:2
|
作者
Gu, Gyo-Jeong [1 ]
Lim, Se-Jin [2 ]
Ahn, Sang-il [1 ]
Lee, Sung-Chan [3 ]
Chang, Young-Tae [4 ,5 ,6 ]
Choi, Tae Hyun [7 ]
Kim, Byoung Soo [7 ]
Eom, Yong-Bin [2 ]
Lee, Na Kyung [2 ]
Youn, Hyung-Sun [1 ,2 ]
机构
[1] Soonchunhyang Univ, Coll Med Sci, Dept Med Sci, Chungnam 336745, Asan Si, South Korea
[2] Soonchunhyang Univ, Coll Med Sci, Dept Biomed Lab Sci, Chungnam 336745, Asan Si, South Korea
[3] Aptabio Therapeut Inc, Yongin 446908, South Korea
[4] Natl Univ Singapore, Inst Life Sci, Dept Chem, Singapore 117543, Singapore
[5] Natl Univ Singapore, Inst Life Sci, MedChem Program, Singapore 117543, Singapore
[6] ASTAR, Singapore Bioimaging Consortium SBIC, Lab Bioimaging Probe Dev, Singapore 138667, Singapore
[7] Korea Inst Radiol & Med Sci, Dept Imaging, Seoul 139706, South Korea
基金
新加坡国家研究基金会;
关键词
Inflammation; Nuclearfactor-kappa B; Cyclooxygenase-2; Inducible nitric oxide synthase; CDr10b; TOLL-LIKE RECEPTOR; NF-KAPPA-B; SIGNALING PATHWAYS; GENE-EXPRESSION; INNATE IMMUNITY; ACTIVATION; TLR4; HOMODIMERIZATION; PHYTOCHEMICALS; RECOGNITION;
D O I
10.1016/j.ejphar.2014.08.036
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The pathophysiological processes of inflammation can lead to a host of diseases, such as periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer. The dysregulated inducible nitric oxide synthase ( iNOS) and cyclooxygenase-2 ( COX- 2) activation play important roles in the development of certain inflammatory diseases. Here, we investigated the effects of CDr10b which is originally developed for a microglia staining probe on inflammation, by modulating NF-kappa B activation and iNOS and COX-2 expression induced by lipopolysaccharide (LPS) in murine macrophages. The CDr10b suppressed NF-kappa B activation and iNOS and COX-2 expression induced by LPS. All the results suggest that CDr10b is a promising novel agent for the treatment of inflammatory diseases. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:42 / 46
页数:5
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