目的 考察沙利度胺对葡聚糖硫酸钠诱导小鼠炎症性肠病的治疗作用,并探讨其可能的作用机制.方法 60只Balb/c小鼠按体质量随机分为对照组、模型组、柳氮磺吡啶(200 mg/kg)组以及沙利度胺30、60、120 mg/kg剂量组,每组10只.试验当天为第1天,试验期间葡聚糖硫酸钠诱导组饮用2.5%葡聚糖硫酸钠饮用水,对照组则饮用纯净水.从试验第5天开始,各给药组开始ig给予相应药物,给药容积10 mL/kg,1次/d,对照组和模型组则给予相应体积的0.5% MC,直至第12天结束试验.试验期间,每天记录各动物体质量变化.试验结束后,测量各动物结肠长度,观察各组结肠组织病理学改变和评分,ELISA法检测结肠组织肿瘤坏死因子-α(TNF-α)含量.结果 沙利度胺在120 mg/kg剂量下改善葡聚糖硫酸钠诱导小鼠体质量下降症状,改善小鼠的结肠缩短,降低结肠组织TNF-α含量,减少炎症细胞对结肠组织的浸润.结论 沙利度胺对葡聚糖硫酸钠诱导小鼠炎症性肠病呈现较好治疗作用,该作用可能与沙利度胺对TNF-α的调节作用有关.

Objective To study the therapeutic effect of thalidomide on dextran sodium sulfate-induced inflammatory bowel disease in mice and explore its possible mechanism. Methods According to body weights, Balb/c mice (60) were randomly divided into control, model, sulfasalazine (200 mg/kg), and thalidomide (30, 60 and 120 mg/kg) groups, and each group had 10 mice. Mice were received 2.5% Dextran sulfate sodium solution for 12 d to induce inflammatory bowel disease except those administered pure water in control group. From fifth day, mice were ig administered thalidomide 30, 60, and 120 mg/kg and sulfasalazine 200 mg/kg with 10 mL/kg and once daily for 7 d, and mice in control and model groups were ig administered corresponding volume of 0.5% MC. During the experiment, body weights were monitored and recorded daily. At the end of experiment, colonic length, pathologic scores, histopathology were evaluated, and tumor necrosis factor-α (TNF-α) levels were determined by ELISA. Results Thalidomide at dose of 120 mg/kg could improve loss of body weight in mice of dextran sodium sulfate-induced inflammatory bowel disease, improve colon shortening, significantly decrease TNF-α levels in colonic tissue, and reduce colon injury of inflammatory cell. Conclusion Thalidomide has therapeutic effect on dextran sodium sulfate-induced inflammatory bowel disease in mice, and the mechanism may be related to regulation of TNF-α levels.