Objective: To investigate the anti-atherosclerotic mechanism of emodin from Polygonum multiflori Radix Praeparata and the effect of Janus kinase 2(JAK2)/signal transduction and activator of transcription 3(STAT3) signaling pathway

and its related factor suppressor of cytokine signaling 3(SOCS3). Method: Eighty male ApoE-/-mice were randomly divided into 8 groups:emodin high

middle

and low dose groups(40

20

10 mg·kg-1)

model group

positive control group(Xuezhikang

200 mg·kg-1)

negative control group(tween-80

4 mg·kg-1)

normal control group

and middle dose of emodin+AG490 group (DA group). In addition to the normal control group

the remaining 7 groups were fed with high-fat diet and subcutaneously injected with lipopolysaccharide

then stopped after 9 weeks. Mice were dosed on the 10th week and sacrificed 6 weeks later. The contents of JAK2

p-JAK2

STAT3

p-STAT3 and SOCS3 were measured by enzyme linked immunosorbent assay(ELISA). The thoracic aorta was stained by hematoxylin and eosin(HE). The expression of JAK2

STAT3 and SOCS3 mRNA was detected by Real-time PCR. Result: Compared with the model group

SOCS3 content increased (P<0.01)

p-JAK2

and p-STAT3 levels decreased(P<0.01) in the emodin high-and middle-dose group

and there was increased in low-dose (P<0.05). There was no change in STAT3

JAK2. The effect of DA in each index was not as good as that in moderate dose group (P<0.01)

but the relative expression of STAT3 in middle dose group was significantly different from that in DA group (P<0.05). The trend of SOCS3 gene expression in each group was increased to that detected by Real-time PCR and the results of JAK2 and STAT3 gene expression were decreased.Under the HE staining microscope

high and middle doses of emodin can effectively delay the formation of atherosclerotic plaque

but the effect of low dose is not obvious. Conclusion: Emodin can significantly affect the development of atherosclerotic lesions in ApoE-/- mice. This mechanism may be related to the inhibition of JAK2/STAT3 signaling pathway.