Objective:

2

To observe the effect of Simiao Yongan Tang on the pathologic morphology of atherosclerosis (AS) vulnerable plaque and the permeability of vasa vasorum (VV)

and to explore its intervention mechanism with VV as the target.

Method:

2

Healthy male ApoE

-/-

mice were randomly divided into model group

Simiao Yongan Tang group(11.7 mg·kg

-1

·d

-1

)and simvastatin group(2.6 mg·kg

-1

·d

-1

). High-fat diet supplemented with 1.1%

L

-methionine was given to induce the animal model

while C57BL/6 mice were used as the control group. The model was evaluated after 8 weeks of feeding. After successful modeling

continued drug intervention was given for 8 weeks

and the pathological changes of the mouse aorta were observed by oil red O staining. The expression levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) proteins in the outer membrane of aortic root plaques were observed by immunohistochemical staining.

Result:

2

The results of oil red O staining showed that as compared with the control group

the plaque area of the aortic wall was significantly increased in the model group (

P

<

0.01). As compared with the model group

the plaque area of the aorta was significantly decreased in the simvastatin group (

P

<

0.01)

end the area of plaque in the aortic wall was reduced in Simiao Yongan Tang group (

P

<

0.05). The results of immunohistochemical staining showed that as compared with the normal control group

the positive expression of MMP-9 in the aortic adventitia was significantly increased in the model group (

P

<

0.01). As compared with the model group

the positive expression of MMP-9 was significantly decreased in simvastatin group and Simiao Yongan Tang group(

P

<

0.01). As compared with the simvastatin group

the positive expression of MMP-9 was significantly decreased in Simiao Yongan Tang group (

P

<

0.01).

Conclusion:

2

Simiao Yongan Tang can reduce the area of mouse aortic plaque

reduce the VV permeability of the outer plaque by regulating the expression of MMP-9 and TIMP-1

and stabilize the vulnerable plaque.