Objective      To study the changes of arterial smooth muscle cells caused by medication of IL-1β through arterial adventitia and their correlation with JAK

2

-STAT

3

signaling pathway

and to clarify the role of JAK

2

-STAT

3

signaling pathway in vascular proliferative diseases.        Methods      Twenty-four SD male rats (6-8 weeks old) of which left common carotid arteries were separated were divided into an experimental group (n=18) and a control group (n=6). In the experimental group

the rats’ vascular adventitia was wrapped with Sepharose suspension containing interleukin-1β (IL-1β) (2.5 μg)

while in the control group (n=6)

the rat’s vascular adventitia were wrapped with Sepharose suspension without IL. At each time point of 2

8

24

48 h

and 1

2 weeks after the operation

3 rats in the experimental group and 1 rat in the control group were sacrificed

respectively. In another 9 SD male rats

both sides of common carotid artery were separated. After a slow-release gel of JAK

2

inhibitor AG490 was dropped on the left side of vascular adventitia and an equivalent blank gel on the right side of vascular adventitia

the same amount of IL-1β was wrapped on both sides. At each time point of 8 and 48 h and 1 week after operation

3 rats were sacrificed

respectively. HE staining was applied to observe the morphology of vascular specimens. The expressions of JAK

2

STAT

3

phospho-JAK

2

(p-JAK

2

) and phospho-STAT

3

(p-STAT

3

) were detected by Western blotting. Immunohistochemical staining was used to locate p-JAK

2

and p-STAT

3

.       Results      The proliferation and migration of vascular smooth muscle cells were observed after the arterial adventitia was wrapped with IL-1β. Western blotting and gray scale analysis showed that relative gray scale value

s of p-JAK

2

were 0.337±0.216 in the control group

1.764±0.513 in the 8 h group

and 0.451±0.229 in the 1 week group. The relative gray scale values of p-STAT

3

were 0.125±0.870 in the control group

1.909±0.309 in the 24 h group

and 0.448±0.516 in the 2 weeks group. There were significant differences of JAK

2

and STAT

3

phosphorylation among different time points (P0.05). After the inhibitor treatment

the relative gray scale values of p-JAK

2

were 0.085±0.031 in the treated side

and 1.416±0.468 in the control side in the 8 h group. The relative gray scale values of p-STAT

3

were 0.460±0.065 in the treated side

and 2.425±0.638 in the control side in the 48 h group. The phosphorylation of JAK

2

and STAT

3

were significantly inhibited (P0.05)

and the changes of smooth muscle cells decreased.        Conclusion      Medication of cytokine IL-1β through arterial adventitia can induce arterial smooth muscle cell proliferation and migration

which are directly associated with JAK

2

-STAT

3

signaling pathway.