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        Sparstolonin B suppresses lipopolysaccharide-induced inflammation in human umbilical vein endothelial cells

        Qiaoli Liang,Fang Yu,Xiaodong Cui,Jin-ao Duan,Qinan Wu,Prakash Nagarkatti,Daping Fan 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.7

        Sparstolonin B (SsnB) is an isocoumarin compoundisolated from the tubers of both Sparganium stoloniferumand Scirpus yagara. We previously demonstratedthat SsnB blocked the Toll-like receptor (TLR) 2- andTLR4-triggered inflammatory signaling in macrophages byinhibiting the recruitment of MyD88 to the TIR domains ofTLR2 and TLR4. The present study was designed toexamine the effects of SsnB on vascular inflammatoryresponses in human umbilical vein endothelial cells (HUVECs)challenged by lipopolysaccharide (LPS, a TLR4ligand). We found that SsnB dose-dependently attenuatedthe LPS-induced expression of interleukin (IL)-1b andmonocyte chemoattractant protein 1 both at the transcriptionand translation levels in HUVEC. LPS-inducedendothelial cell adhesion molecules, intercellular adhesionmolecular-1 and vascular cell adhesion molecule-1expressions were also reduced by treatment with SsnB. Inaddition, co-incubation with SsnB attenuated THP-1monocyte adhesion to LPS-activated HUVECs. Furthermore,SsnB efficiently suppressed LPS-induced phosphorylationof extracellular -signal-regulated kinase (Erk1/2)and Akt in HUVECs. These findings show that SsnB cansuppress endothelial cell inflammation, suggesting thatSsnB might be suitable for development as a therapeuticagent for inflammatory cardiovascular disease.

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