Suffrutines A and B Inhibit the Expression of Inflammatory Mediators in LPS-Induced RAW264.7 Cells by Suppressing the NF-κB Signaling Pathway

被引:0
作者
Chen, Chun [1 ]
Zhu, Ze-Feng [1 ,2 ]
Nie, Wen-Xing [1 ]
Zou, Yong [1 ,3 ]
机构
[1] Sun Yat Sen Univ, Sch Pharmaceut Sci, 132 Waihuan East Rd, Guangzhou, Guangdong, Peoples R China
[2] Jinan Univ, Affiliated Hosp 1, Dept Pharm, Heyuan, Guangdong, Peoples R China
[3] Guangdong Prov Key Lab Chiral Mol & Drug Discover, Guangzhou, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Euphorbiaceae; Flueggea suffruticosa; inflammatory mediators; NF-kappa B signaling pathway; RAW264.7; suffrutines A; suffrutines B; CYCLOOXYGENASE-2; PRINCIPLES; ACTIVATION; ALKALOIDS;
D O I
10.1055/a-1528-1760
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Flueggea suffruticosa is a traditional Chinese medicine that has been commonly used for the treatment of inflammatory ailments, including rheumatism and lumbago. Suffrutines A and suffrutines B are a pair of novel E,E and Z,E isomeric indolizidine alkaloids isolated from the roots of F. suffruticosa. However, their anti- inflammatory activity has not been reported thus far. The aim of this study was to investigate the inhibitory effect of inflammatory mediators and possible mechanisms of suffrutines A and B in lipopolysaccharide-induced RAW264.7 cells. Results showed that suffrutines A and B could remarkably inhibit the production of nitric oxide, prostaglandin E-2, interleukin-6, inducible nitric oxide synthase, and cyclooxygenase-2 in lipopolysaccharide-induced RAW264.7 cells. Further evaluation demonstrated that compared with suffrutines A, suffrutines B could more significantly inhibit the phosphorylation of IKK alpha/beta, the degradation of I kappa B alpha, and the nuclear translocation of the p65 and p52 subunits in the canonical and non-canonical nuclear factor-kappa B pathways. Therefore, suffrutines B exhibited more potent inhibitory activity on inflammatory mediators than suffrutines A.
引用
收藏
页码:628 / 638
页数:11
相关论文
共 33 条
[1]   NF-κB, Inflammation, and Metabolic Disease [J].
Baker, Rebecca G. ;
Hayden, Matthew S. ;
Ghosh, Sankar .
CELL METABOLISM, 2011, 13 (01) :11-22
[2]  
Chirkin E., 2015, ALKALOIDS, V74, P1, DOI DOI 10.1016/BS.ALKAL.2014.11.001
[3]   Inflammation: A Multidimensional Insight on Natural Anti-Inflammatory Therapeutic Compounds [J].
Dar, Khalid Bashir ;
Bhat, Aashiq Hussain ;
Amin, Shajrul ;
Masood, Akbar ;
Zargar, Mohammad Afzal ;
Ganie, Showkat Ahmad .
CURRENT MEDICINAL CHEMISTRY, 2016, 23 (33) :3775-3800
[4]   Melatonin suppresses macrophage cyclooxygenase-2 and inducible nitric oxide synthase expression by inhibiting p52 acetylation and binding [J].
Deng, Wu-Guo ;
Tang, Shao-Tzu ;
Tseng, Hui-Ping ;
Wu, Kenneth K. .
BLOOD, 2006, 108 (02) :518-524
[5]  
Dhingra Ashwani Kumar, 2015, Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry, V14, P81, DOI 10.2174/1871523014666150514102027
[6]  
Editorial Committee of Nanjing Pharmaceutical College, 1976, CHINESE HERBAL MED, P599
[7]   Oncogenic inflammation and autoimmune disease [J].
Eisenlohr, Laurence C. ;
Rothstein, Jay L. .
AUTOIMMUNITY REVIEWS, 2006, 6 (02) :107-114
[8]   Quercetin disrupts tyrosine-phosphorylated phosphatidylinositol 3-kinase and myeloid differentiation factor-88 association, and inhibits MAPK/AP-1 and IKK/NF-κB-induced inflammatory mediators production in RAW 264.7 cells [J].
Endale, Mehari ;
Park, Seung-Chun ;
Kim, Suk ;
Kim, Seung-Hyung ;
Yang, Yanyan ;
Cho, Jae Youl ;
Rhee, Man Hee .
IMMUNOBIOLOGY, 2013, 218 (12) :1452-1467
[9]   Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes [J].
Esser, Nathalie ;
Legrand-Poels, Sylvie ;
Piette, Jacques ;
Scheen, Andre J. ;
Paquot, Nicolas .
DIABETES RESEARCH AND CLINICAL PRACTICE, 2014, 105 (02) :141-150
[10]   Introduction to NF-κB:: players, pathways, perspectives [J].
Gilmore, T. D. .
ONCOGENE, 2006, 25 (51) :6680-6684