大鼠实验性溃疡性结肠炎中NO、MDA、SOD的变化

目的 :建立大鼠实验性溃疡性结肠炎的模型 ,观察结肠组织中NO、MDA、SOD的变化。方法 :30只Wistar大鼠 ,随机分为正常对照组、实验组、治疗组各 10只 ,实验组和治疗组用乙酸灌肠建立大鼠溃疡性结肠炎的模型后 ,分别给予生理盐水、SASP 80mg/(kg·d)各 1ml/d灌肠 ,采用组织病理学进行损伤指数评分 ;生化法检测组织中NO、MDA、SOD值。结果 :实验组NO[(5 .19± 0 .4 5 ) μmol/g蛋白 ]、MDA[(30 .6± 2 .18)nmol/g蛋白 ]均显著增高于对照组 [(1.96± 0 .2 9) μmol/g蛋白 ,(6 .82± 0 .81)nmol/g蛋白 ,P <0 .0 1]、治疗组 [(2 .98± 0 .2 7) μmol/g蛋白 ,(14 .79± 1.92 )nmol/g蛋白 ,P <0 .0 1) ];实验组 [SOD(11.0 6± 1.82 )U/g蛋白 ]显著降低于对照组 [(2 2 .2± 1.6 2 )U/g蛋白 ,P <0 .0 1]、治疗组 [(17.7± 1.76 )U/g蛋白 ,P <0 .0 1],实验组的损伤指数 (3.89± 0 .78)显著高于治疗组 (1.30± 0 .4 8,P<0 .0 1)。治疗组与对照组各值比较也有显著性差异 (P <0 .0 1)。结论 :自由基参与溃疡性结肠炎的病理过程 ,降低自由基水平可以为治疗溃疡性结肠炎提供新的途径

Change of NO,MDA and SOD in Experimental Ulceritive Colitis in Rats

Objective: To estabilish rat ulcerative colitis model and observe abnormal NO,MDA,SOD in colon constitution. Methods: 30 Wister rats were divided into 3 groups:nomal control,experiment and treatment,which in latter two groups were respectively received saline enemas, SASP 80 mg/(kg·d) enemas 1 ml daily after distal colitis was induced by 8% acetic acid enemas was studed by histopatholog and biochemistry,respectively. Results: NO[(5.19±0.45)μmol/g pro], MDA[(30.6±2.18)nmol/g pro] in experiment group was significantly increased than that in control group[(1.96±0.29)μmol/g pro,(6.82±0.81)nmol/g pro,[WTBX]P<0.01)]and treatment group and treatment group [(2.98±0.27)μmol/g pro,(14.79±1.92)nmol/g pro,[WTBX]P<0.01].But SOD.But SOD[(11.06±1.82)u/g pro] in experiment group was significantly lower than that in control group[(22.2±1.62)u/g pro,P<0.01]and treatment group[(17.7±1.76)u/g pro,[WTBX]P<0.01]. The damage score (3.89±0.78)in experiment group was notably higher than that in treatment group(1.30±0.48,. The damage score (3.89±0.78)in experiment group was notably higher than that in treatment group(1.30±0.48,P<0.01)). There were also significant difference between treatment group and control group (P<0.01). Concolusion: To reduce free radical which involved in the pathological process of the disease can provide a new pathway for therapy ulcerative colitis.