Objective: To investigate the effects of microRNA-520b(miR-520b) associated with blood stasis syndrome on interleukin-8(IL-8) and the intervention of tanshinone ⅡA(Tan ⅡA). Method: Synthetic miR-520b mimic(50 nmol · L-1) or inhibitor (100 nmol · L-1) were transfected into 1.6×104 cells/well human umbilical venous endothelial cells (HUVECs) 24

36

48 h by lipofectamineTM 2000 and then

5

10

20

40 mg ·L-1 Tan ⅡA intervented miR520b-transfected HUVECs 24

48 h. The proliferation(n=5) and nitric oxide(NO)

endothelial protein C receptor(EPCR)

Von Willebrand factor(vWF)

thrombomodulin(TM) and endothelin(ET)' s concentration of HUVECs were analyzed by MTT assay

nitrate reduction assay and ELISA assay respectively(n=3). Transfection efficiency of miR-520b was detected by the fluorescence microscope and IL-8 mRNA and protein were also detected(n=3). Result: Compared with normal group

miR-520b inhibited the proliferation and NO concentration

and promoted the EPCR

vWF

and ET concentration of HUVECs in the miR-520b group. After 48 hours

the expression of IL-8 mRNA and protein were significantly decreased in miR-520b group. Tan ⅡA increased significantly the proliferation and NO concentration

and decreased significantly the EPCR

vWF

TM and ET concentration of HUVECs. Additionally

the expression of IL-8 mRNA and protein were significantly increased in the Tan ⅡA group

in comparison to the miR-520b group. Conclusion: MicroRNA-520b may promote the development of blood stasis syndrome in HUVECs by inhibiting the expression of IL-8. This process may be reversed by Tan ⅡA.