Abstract

Objective To explore mechanism of molecule of glycyrrhizinate and 5-aminosalicylic acid(5-ASA) treating ulcerative colitis(UC) through observing expression of TNF-α,IL-8 and NF-κB in rats with UC induced by 2,4-dinitro-chlorobenzene and acetic acid. Method 50 male Wistar rats were randomly divided into 5 groups: normal control group, UC model group,5-ASA group, glycyrrhizinate group and unification medication group.(10 rats in each group). The rats in normal control group and UC model group were given normal saline, the rats in 5-ASA group were given 5-ASA (1ml/200g weight), the rats in glycyrrhizinate group were given glycyrrhizinate(1ml/200g weight), the rats in unification medication group were given 5-ASA(1ml/200g weight) and glycyrrhizinate(1ml/200g weight). Symptom of bowel complaint and hemafecia in rats was observed and the change of body weight was recorded every day.After 7 days, blood of rats were got, the level of TNF-α、IL-8 in the blood serum was evaluated by ELISA. Colons(8cm) of rats were got, score of colonic damage was determined, the level of NF-κB in colonic mucosa was determined by immunohistochemistry. Result In the stage of UC, score of colonic damage advanced obviously, the level of TNF-α,IL-8 in the blood serum and expression of NF-κB in colonic mucosa advanced obviously, and those were correlated with change of state of the illness; After using glycyrrhizinate or 5-ASA, score of colonic damage in every group degraded obviously, the level of TNF-α,IL-8 in the blood serum and expression of NF-κB in colonic mucosa descended obviously; The effects of unification medication of glycyrrhizinate and 5-ASA lowering the level of TNF-α,IL-8 in the blood serum and expression of NF-κB in colonic mucosa were more excellent than that of single sentero clyster by using 5-aminosalicylic acid or glycyrrhizinate (P<0.05) . Conclusion Unification utilizing glycyrrhizinate and 5-ASA had a good therapeutic action for rats with ulcerative colitis evoked by 2,4-Dinitro-chlorobenzene and acetic acid. Its mechanism of action might be to reduce damage of inflammation by suppressing of expression of TNF-α,IL-8 and NF-κB in rats .

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