目的 考察沙利度胺對(duì)葡聚糖硫酸鈉誘導(dǎo)小鼠炎癥性腸病的治療作用,并探討其可能的作用機(jī)制.方法 60只Balb/c小鼠按體質(zhì)量隨機(jī)分為對(duì)照組、模型組、柳氮磺吡啶(200 mg/kg)組以及沙利度胺30、60、120 mg/kg劑量組,每組10只.試驗(yàn)當(dāng)天為第1天,試驗(yàn)期間葡聚糖硫酸鈉誘導(dǎo)組飲用2.5%葡聚糖硫酸鈉飲用水,對(duì)照組則飲用純凈水.從試驗(yàn)第5天開(kāi)始,各給藥組開(kāi)始ig給予相應(yīng)藥物,給藥容積10 mL/kg,1次/d,對(duì)照組和模型組則給予相應(yīng)體積的0.5% MC,直至第12天結(jié)束試驗(yàn).試驗(yàn)期間,每天記錄各動(dòng)物體質(zhì)量變化.試驗(yàn)結(jié)束后,測(cè)量各動(dòng)物結(jié)腸長(zhǎng)度,觀察各組結(jié)腸組織病理學(xué)改變和評(píng)分,ELISA法檢測(cè)結(jié)腸組織腫瘤壞死因子-α(TNF-α)含量.結(jié)果 沙利度胺在120 mg/kg劑量下改善葡聚糖硫酸鈉誘導(dǎo)小鼠體質(zhì)量下降癥狀,改善小鼠的結(jié)腸縮短,降低結(jié)腸組織TNF-α含量,減少炎癥細(xì)胞對(duì)結(jié)腸組織的浸潤(rùn).結(jié)論 沙利度胺對(duì)葡聚糖硫酸鈉誘導(dǎo)小鼠炎癥性腸病呈現(xiàn)較好治療作用,該作用可能與沙利度胺對(duì)TNF-α的調(diào)節(jié)作用有關(guān).

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.