Objective       To determine the therapeutic effect of emodin on carotid artery stenosis

and explore its underlying mechanism. Methods     Seventy-two SD rats (200 g) were randomly divided into 3 groups

sham operation group (n=24)

injury group (n=24)

and emodin treatment group (n=24). For the rats from the injury group and emodin treatment group

the carotid artery stenosis model was established with a balloon catheter (2.0 mm×12 mm). The sham operation group was in agreement with the other 2 groups except balloon injury. In the emodin treatment group

emodin (70 mg/kg) was given intragastrically

and the other 2 groups were given with the equal-volume of solvents (DMSO in normal saline). In 14 d later

the carotid arteries were isolated from the 3 groups of rats for pathological observation after HE staining

for the content of reactive oxygen species (ROS) by the dihydroethidium (DHE) measurement

and for the expression of α-smooth muscle actin (α-SMA)

c-myc and Ki67 by immunohistochemical staining. Western blotting was used to measure the contents of MEK1/2

p-MEK1/2

ERK1/2

p-ERK1/2 and nuclear c-myc in the cell plasma. Results       HE staining displayed that the model of carotid artery stenosis was successfully established

and the hyperplasia of neointimal was significantly fastest  in 14 d in comparison with 3 and 7 d (P0.01). The main component of the neointimal was vascular smooth muscle cells (VSMCs). Compared with the sham operation group

the level of ROS was significantly increased in the injury group (P0.01)

while emodin treatment obviously reduced the ROS level (P0.01). Compared with the injury group

emodin significantly inhibited the expression of Ki67 (P0.01)

reduced the activation of MAPK-ERK pathway and decreased the activation of nuclear c-myc (P0.01). Conclusion       Emodin alleviates rat carotid artery stenosis

which may be due to its down-regulation the activation ROS/MAPK/ERK/c-myc signal pathway

decrease of Ki67 protein expression

and thus suppresses the excessive proliferation of neointimal VSMCs.