Objective:To study the mechanism of oxymatrine treating ulcer colitis（UC）in rats.Method: SPF rats were randomly divided into normal group

UC model group

oxymatrine +UC group（oxymatrine 180 mg·kg-1

ig）

sulfasalazine+UC model group（sulfasalazine 600 mg·kg-1

ig）

2

4

6-trinitrobenzene sulfonic acid（TNBS） was used to induce rat ulcer colitis model

and corresponding drugs were given for 21 d.after 21 days of administration

colitis were collected

immunohistochemistry method was used to detect expression of κBα（IκB-α） protein in colon tissue

while the expression of tumor necrosis-factor-α（TNF-α）

interleukin（IL）-1β

IL-6

IL-8 cytokines were measured in each colonic tissue

and microscopic examination of colonic biopsy were carried out.Result: IκB-α protein expressions in oxymatrine group 21.8%±5.0% was significantly lower than that of model group 25.6%±2.9%（P<0.01）;and the expressions of TNF-α（66.23 ±2.64）pg·mg-1

IL-1β（149.42 ±64.69）pg·mg-1

IL-6（668.83±98.11）pg·mg-1and IL-8（91.83±23.1 4） pg·mg-1was significantly decreased（P<0.05）

compared with model group.Microscopic examination of colon tissue showed that the colonic inflammation

lymphocyte infiltration

mucosal damage in treatment group were significantly better than these of model group.Conclusion: Oxymatrine has anti-inflammatory effect by interfering with the IκB-α protein expression

and inhibiting the nuclear transcription factor κB（nuclear transcription factor-kappaB

NF-κB） activity in colitiscells.