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Title 

Ephedrannin A and B from roots of Ephedra sinica inhibit lipopolysaccharide-induced inflammatory mediators by suppressing nuclear factor-κB activation in RAW 264.7 macrophages

 

마황근의 에페드라닌의 염증반응 억제효과

Authors 

I S KimYoung-Jun ParkSung-Jin YoonH B Lee

Publisher 

Elsevier

Issue Date 

2010

Citation 

International Immunopharmacology, vol. 10, no. 12, pp. 1616-1625

Keywords 

CytokinesEphedra sinicaEphedrannin AEphedrannin BInflammationNuclear factor-kappa B (NF-κB)

Abstract 

Ephedra sinica is a traditional Chinese medicinal herb and has pharmacological functions including anti-inflammatory effects. However, the active ingredients from Ephedra roots have not been characterized. Here, two active constituents were isolated and their structures and mechanisms of action were defined. Active constituents from Ephedra roots were isolated by continuous solvent-extractions and column chromatography. Their structures were determined by use of multiple types of spectrometry. The mechanisms of action were examined using lipopolysaccharide (LPS)-stimulated RAW 264.7 cells through PCR, ELISA, electrophoretic mobility shift assays, and immunocytochemistry. Two active constituents, ephedrannin A and B, belonging to the A-type proanthocyanidin family were identified. Both ephedrannin A and B effectively suppressed the transcription of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). These compounds exerted their anti-inflammatory actions on LPS-stimulated macrophages by suppressing the translocation of nuclear factor-kappa B (NF-κB) and the phosphorylation of p38 mitogen-activated protein (MAP) kinase. Ephedrannin A and B both exhibited strong anti-inflammatory effects, however, the optimal dose of ephedrannin B was 10 times lower than that of ephedrannin A. This is the first report describing effective anti-inflammatory activity for ephedrannin A and B isolated from Ephedra roots. Ephedrannin B may be a good candidate for delaying the progression of human inflammatory diseases and warrants further studies.

ISSN 

1567-5769

Link 

http://dx.doi.org/10.1016/j.intimp.2010.09.019

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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