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目的:观察不同剂量白花蛇舌草总黄酮(FOD)对小鼠产生的溃疡性结肠炎(UC)的防治作用,并初步探讨其作用机制。方法:60只小鼠随机分为6组(n=10):正常对照组、模型组、柳氮磺胺吡啶(SASP)治疗组、FOD高、中、低剂量治疗组。正常对照组一直饮用纯化水,后5组自由饮用4%右旋葡聚糖硫酸钠(DSS)水溶液代替日常饮用水制备UC小鼠模型;造模同时,SASP治疗组灌胃SASP500mg.kg-1.d-1,FOD高、中、低剂量治疗组灌胃FOD分别为60,40,26.7mg.kg-1.d-1,正常对照组和模型组每天灌服等量生理盐水作对照。每天观察各组小鼠的临床症状,喂养7d后处死小鼠取结肠组织,观察结肠黏膜损伤情况,同时检测结肠组织中超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性、丙二醛(MDA)和一氧化氮(NO)含量。结果:与模型组比较,FOD高、中剂量治疗组症状不同程度的明显改善、结肠黏膜损伤减轻;结肠组织中SOD活性明显升高(P<0.05),MPO、MDA、NO活性或含量不同程度的明显降低(P<0.05);FOD高剂量治疗组与SASP治疗组作用相似。结论:FOD对小鼠UC作用显著,其机制可能与减少自由基生成、抑制脂质过氧化反应和增强抗氧化能力作用有关。
OBJECTIVE: To observe the preventive and therapeutic effects of different doses of total flavonoids of Hedyotic diffusa (FOD) on ulcerative colitis (UC) induced by mice and to explore its mechanism. Methods: Sixty mice were randomly divided into 6 groups (n = 10): normal control group, model group, sulfasalazine (SASP) treatment group, high, medium and low dose FOD treatment group. The normal control group had been drinking purified water. After 5 groups were free to drink 4% dextran sodium sulfate (DSS) aqueous solution instead of daily drinking water preparation UC mouse model; modeling at the same time, SASP treatment group intragastric administration of SASP500mg.kg-1 .d-1, FOD in high, medium and low dose FOD groups were respectively 60, 40, 26.7 mg.kg-1.d-1, the normal control group and model group were given the same amount of normal saline as control. The clinical symptoms of mice in each group were observed daily. After 7 days of feeding, the colon tissues were sacrificed and the colonic mucosal damage was observed. The activity of superoxide dismutase (SOD) and myeloperoxidase (MPO) Dialdehyde (MDA) and nitric oxide (NO) content. Results: Compared with model group, the symptom of high and medium dose FOD groups improved obviously, the damage of colonic mucosa was lessened; the activity of SOD in colon tissue was significantly increased (P <0.05); the activity or content of MPO, MDA and NO were different (P <0.05). The effect of high dose FOD treatment group was similar to that of SASP treatment group. Conclusion: FOD has a significant effect on UC in mice. The mechanism may be related to the reduction of free radical generation, inhibition of lipid peroxidation and enhancement of antioxidant capacity.