Objective: To observe the effect of Shaoyaotang on colon tissues JAK2/STAT3 and SOCS3

in order to discuss the mechanism of Shaoyaotang by treating the rat model of syndrome type ulcerative colitis (UC). Method: A total of 120 Wistar rats

including 60 male rats and 60 female rats

were divided into 6 groups:blank group

model group

high-dose (24 g·kg-1)

medium-dose (12 g·kg-1)

low-dose (6 g·kg-1) Shaoyaotang groups

and western medicine group (sulfasalazine group

1 g·kg-1). High-fat

high-sugar

spicy food plus immune complex

TBNS (2

4

6-trinitro-benzene-sulfonic acid) and ethanol were used to replicate the syndrome type UC rat model. Wistar rats in different groups were given different treatments for consecutively 21 days. In Shaoyaotang group

Wistar rats were given high

medium and low-dose Shaoyaotang by gavage. In western medicine group

they were administered with sulfasalazine powder. In blank group and model group

they were given isopyknic normal saline for intragastric administration. After collecting abdominal aorta serum and colon tissues

sue-eosin methyl (HE) staining was used to observe the pathological section; Real-time PCR method was used to detect the contents of genes. And Western blot method was used to detect the contents of protein. Result: The model group showed inflammatory reaction

mucosa damage and ulceration under the endoscope

which indicated the successful modeling. Compared with blank group

model group's JAK2 and STAT3 protein and gene expressions increased significantly (P<0.05)

while SOCS3 decreased significantly (P<0.05). Compared with the model group

in Shaoyaotang treatment groups

JAK2 and STAT3 protein and gene expressions were significantly decreased

and high-dose Shaoyaotang group showed the most obvious effect (P<0.01); SOCS3 increased dramatically

and high-dose Shaoyaotang group showed the most obvious effect (P<0.05). Conclusion: Shaoyaotang can improve the pathological changes in colon mucosal tissues of rats with syndrome type UC and reduce inflammation

which may be related to the inhibition of JAK/STAT3 signaling pathway by SOCS3

the generation of negative feedback regulation and the decrease in activation.