Effusanin E

Antibacterial activity-guided purification and identification of a novel C-20 oxygenated ent-kaurane from Rabdosia serra (MAXIM.) HARA.[Pubmed:23561188]

Food Chem. 2013 Aug 15;139(1-4):902-9.

The objective of this work was to conduct an activity-guided isolation of antibacterial compounds from Rabdosia serra. The ethanol extracts of R. serra leaf and stem were partitioned sequentially into petroleum ether, ethyl acetate, butanol and water fractions, respectively. The ethanol extract of leaf evidenced broad-spectrum antibacterial activity against gram-positive bacterial, including Bacillus subtilis, Bacillus cereus, Staphylococcus aureus, and Listeria monocytogenes. The ethyl acetate fractions of leaf and stem exhibited strong inhibition against gram-positive bacteria, and were then purified further. On the basis of antibacterial assay-guided purification, three phenolic compounds (rosmarinic acid, methyl rosmarinate and pedalitin) and four C-20 oxygenated ent-kauranes (Effusanin E, lasiodin, rabdosichuanin D and a new compound namely effusanin F) were obtained, whose contents were determined by HPLC analysis. The broth microdilution method confirmed the important inhibition potential of C-20 oxygenated ent-kauranes with low minimum inhibitory concentration (MIC) values. Effusanin E, lasiodin and effusanin F could be useful for the development of new antibacterial agents.

Effusanin E suppresses nasopharyngeal carcinoma cell growth by inhibiting NF-kappaB and COX-2 signaling.[Pubmed:25333664]

PLoS One. 2014 Oct 21;9(10):e109951.

Rabdosia serra is well known for its antibacterial, anti-inflammatory and antitumor activities, but no information has been available for the active compounds derived from this plant in inhibiting human nasopharyngeal carcinoma (NPC) cell growth. In this study, we isolated and purified a natural diterpenoid from Rabdosia serra and identified its chemical structure as Effusanin E and elucidated its underlying mechanism of action in inhibiting NPC cell growth. Effusanin E significantly inhibited cell proliferation and induced apoptosis in NPC cells. Effusanin E also induced the cleavage of PARP, caspase-3 and -9 proteins and inhibited the nuclear translocation of p65 NF-kappaB proteins. Moreover, Effusanin E abrogated the binding of NF-kappaB to the COX-2 promoter, thereby inhibiting the expression and promoter activity of COX-2. Pretreatment with a COX-2 or NF-kappaB-selective inhibitor (celecoxib or ammonium pyrrolidinedithiocarbamate) had an additive effect on the Effusanin E-mediated inhibition of proliferation, while pretreatment with an activator of NF-kappaB/COX-2 (lipopolysaccharides) abrogated the Effusanin E-mediated inhibition of proliferation. Effusanin E also significantly suppressed tumor growth in a xenograft mouse model without obvious toxicity, furthermore, the expression of p50 NF-kappaB and COX-2 were down-regulated in the tumors of nude mice. These data suggest that Effusanin E suppresses p50/p65 proteins to down-regulate COX-2 expression, thereby inhibiting NPC cell growth. Our findings provide new insights into exploring Effusanin E as a potential therapeutic compound for the treatment of human nasopharyngeal carcinoma.