Objective:To investigate the anti-atherosclerosis mechanism of Sanhuang Xiexintang in activating blood and resolving stasis (SXTAR) in vitro. Method:The cell injury model was established with oxidized law-density lipoprotein(ox-LDL) in cultured human umbilical vein endothelial cells live (HUVECs) in vitro

and divided into control group

model group

and SXTAR 15.63

31.25

62.50 mg·L-1 groups. The HUVECs livability and the concerning markers in cell supernatant

like malondialdehyde(MDA)

monocyte chemoattractant protein-1(MCP-1)

intercellular adhesion molecule-1(ICAM-1)

vascular cell adhesion molecule-1(VCAM-1)

superoxide dismutase(SOD) and nitric oxide(NO)

were detected; reactive oxygen species(ROS) was measured by fluorescence quantitation. Apoptosis rate and mitochondrial membrane potential were determined by flow cytometry. Western blot was employed for testing expressions of B-cell lymphoma-2(Bcl-2)

Bcl-2 associated X protein(Bax)

cysteine aspartate-specific protease-3(Caspase-3). Result:The survival rate of HUVECs in model group was significantly lower than that of control group. In the model group

MDA

MCP-1

ICAM-1

VCAM-1 were significant increases

SOD and NO content were decreased

apoptosis rate

ROS and expressions of Bax

Caspase-3

Caspase-9 were up-regulated

and expression of Bcl-2 was down(P<0.05

P<0.01)-regulated. SXTAR significantly increased the survival rate of HUVECs. Compared with the model group

SXTAR significantly decreased contents of MDA

MCP-1

ICAM-1 and VCAM-1.SOD and NO content were increased

apoptosis rate

ROS and expressions of Bax

Caspase-3

Caspase-9 was down-regulated

and expression of Bcl-2 was up-regulated(P<0.05

P<0.01). Conclusion:SXTAR can protect HUVECs injured by ox-LDL

which may be related with inhibiting the endothelial cell apoptosis

reducing inflammation and resisting oxidation.