Objective: To explore the curative effect of Tongxie Yaofang on ulcerative colitis (UC) in rat hypothalamus cytokine interleukin-6 (IL-6) and interleukin-6 receptors (IL-6R) gene and protein expressions. Method: After the ulcerative colitis model was established by the composite method. SPF Wistar rats were randomly divided into 5 groups: model group

low

middle

high-dose Tongxie Yaofang groups (2.75

5.5

11 g·kg-1)

and 5-ASA group. After modeling

rats were given drugs for 21 days. Then

colonic mucosa damage was observed. The levels of IL-6 in the serum tissues were detected by enzyme linked immunosorbent assay (ELISA). The proteins expressions of IL-6 and IL-6R in rat hypothalamus tissues were detected by immunohistochemistry

and their gene expressions were measured by Real-time PCR method. Result: ELISA test results show that compared with control group

model group showed significant increase in content of IL-6 in serum of rats. After drug treatment

the serum IL-6 in drug group were decreased

with the most obvious effect in high-dose Tongxie Yaofang group (P<0.05). Real-time PCR results showed that model group's hypothalamic IL-6 and IL-6R gene expressions were higher than those of blank group (P<0.05). After treatment with drugs

drug group's IL-6 and IL-6R gene expressions were reduced

and 5-ASA and high-dose Tongxie Yaofang groups were superior to the other groups (P<0.05). Immunohistochemical staining results showed that compared with control group

IL-6 and IL-6R protein expressions of ulcerative colitis rats increased significantly (P<0.05)

drug treatment can reduce their hypothalamic IL-6 and IL-6R protein expressions

and 5-ASA and high-dose Tongxie Yaofang groups were superior to the other groups (P<0.05). Conclusion: Tongxie Yaofang can obviously inhibit IL-6 and IL-6R gene and protein expressions in hypothalamic tissues of the rat UC model by TNBS/ethanol method

suggesting Tongxie Yaofang's mechanism in the treatment of ulcerative colitis may be correlated with inhibition of abnormal activation of IL-6/IL-6R signaling pathway in hypothalamus.