Objective: To study the effect and mechanism of sodium tanshinone ⅡA sulfonate (STS) on human umbilical vein endothelial cell(HUVEC) inflammatory injury by visfatin. Method: The human umbilical vein endothelial cells (HUVECs) were cultured in vitro

after the cells were treated with visfatin(250 μg·L-1)for 4 hours

STS was added to the cells in different concentration of(30

60

120 mg·L-1) for 24 hours. The levels of inflammatory cytokines as high sensitivity C reactive protein(hs-CRP)

tumor necrosis factor α(TNF-α)and metal matrix protein (MMP)-9 were determined by enzyme-linked immunosorbent assay(ELISA). The activation of mitogen-activated protein kinases(MAPKs) was assayed by Western blotting. In order to evaluate the role of MAPKs in the inflammatory injury by visfatin

HUVECs were pretreated with MAPKs inhibitor

and visfatin was added after the pretreatment

then the levels of hs-CRP

TNF-α and MMP-9 was measured. Result: Visfatin led to an increase level of hs-CRP

TNF-α and MMP-9

while the increase of above mentioned cytokines induced by visfatin could be inhibited by STS in a dose dependent way. STS could also inhibit the activation of p38 MAPK and extracellular signalregulated kinase (ERK)

but no significant inhibition of Jun N-terminal kinase(JNK). The p38 MAPK inhibitor SB203580(25 μmol·L-1)

ERK inhibitor PD98059 (25 μmol·L-1) and JNK inhibitor SP600125(25 μmol·L-1) markedly decreased visfatin-induced enhance in hs-CRP

TNF-α and MMP-9 expression. Conclusion: Inflammatory response of HUVEC could be induced by visfatin

the mechanism may be related to high expression of inflammatory cytokines

which may be mediated by MAPK phosphorylation signaling pathway. STS attenuates visfatin-induced inflammatory injury by interfering with the modulation of MAPK signal pathway.