Objective: To research the preventive effect and mechanism of Coptidis Rhizoma and Zingiberis Rhizoma(CRZR) in dextran sulphate sodium salt (DSS)-induced colitis model. Method: Totally 45 C57BL/6 mice were randomly assigned to blank control group (normal mice

n=9)

model group (colitis mice

n=9)

CRZR low dose group (1.2 mg·kg-1

n=9)

CRZR middle dose group (2.4 mg·kg-1

n=9) and CRZR high dose group (4.8 mg·kg-1

n=9). After preventive treatment in CRZR groups by intragastric administration for 7 days (same volume of normal saline in normal group and model group)

free drinking of 3%DSS solution was given in model group and Chinese medicine group for 6 days and the tap water was given in normal group. The body weights

stool consistency

and blood in the stool were monitored every day to calculate the disease activity index (DAI). The mice were sacrificed on day 7

and the colons (from the ileocecal junction to the anal verge) were removed and the length was measured. htoxylin-eosin(HE) staining was used to observe the pathological changes of colon and the histopathological scores were recorded; enzymelinked immunosorbent assay(ELISA) was used to detect interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) in plasma of mice; Western blot was used to detect JAK2 and STAT3 protein phosphorylation levels in colonic epithelial cells; and confocal laser scanning microscopy was used to detect the phosphorylated STAT3 (p-STAT3) expression level in colonic tissues. Result: DSS-induced model mice had an increased DAI score and decreased colon length as compared with the normal mice. CRZR low dose group had obviously lower DAI scores on day 2

4

6 and longer colon length as compared with the model group; CRZR middle dose group had lower DAI scores except day 4 and longer colon length as compared with the model group; CRZR high dose group had lower DAI scores from day 2 to end of the experiment and longer colon length as compared with the model group (P<0.05). HE staining showed that the inflammatory injury in the model group was significantly more severe than that in the normal group

and the inflammatory injury in CRZR groups was significantly milder than that in model group; the pathological score in model group was significantly higher than that in normal group (P<0.01)

and the pathological scores in CRZR middle dose and high dose groups were significantly lower than that in the model group (P<0.05). The levels of IL-6 and TNF-α in plasma of model group were significantly higher than those in normal group (P<0.01)

and the levels in CRZR groups were significantly lower than those in model group (P<0.01). JAK2 and STAT3 protein activation levels in colonic tissues in model group were significantly higher than those in normal group (P<0.01)

and the levels in CRZR groups were lower than those in model group (P<0.01

P<0.05). Conclusion: These results indicated that CRZR may prevent DSS-induced colitis and colonic inflammation by inhibiting IL-6/STAT3 signaling pathway.