摘要
背景:溃疡性结肠炎(UC)是一种病因未明的结直肠炎症,大蒜素对其防治的作用目前尚未有结论。目的:探讨大蒜素对TNBS诱导的大鼠结肠炎的保护作用及其机制。方法:80只大鼠随机分为对照组、TNBS组、大蒜素预防组、大蒜素灌胃组、大蒜素灌肠组、地塞米松组、柳氮磺吡啶组、巴柳氮钠组。以含150 mg/kg TNBS的50%乙醇溶液灌肠制备大鼠结肠炎模型。造模2周后处死大鼠。行大体评分和病理学评分,以ELISA法测定血清TNF-α、IL-1β、IL-10、IL-4含量,蛋白质印迹法检测NF-κB表达。结果:与对照组相比,TNBS组大体和病理学评分均明显升高(P<0.05),体质量明显降低(P<0.05),血清TNF-α、IL-1β含量显著升高(P<0.05),血清IL-4、IL-10含量显著降低(P<0.05),NF-κB表达明显升高(P<0.05);给予大蒜素预防或治疗后,上述指标均明显改善(P<0.05),但疗效低于地塞米松组、柳氮磺吡啶组、巴柳氮钠组。结论:大蒜素对TNBS诱导的大鼠结肠炎有保护作用,可能是通过调控细胞因子和NF-κB而发挥作用的。
Background： Ulcerative colitis （UC） is a disease of colorectal inflammation with unknown etiology, the protective effect of diallyl trisulfide （DATS） on UC is still controversial. Aims： To explore the protective role and mechanism of DATS in TNBS-induced colitis in rats. Methods： Eighty rats were randomly divided into 8 groups： control group, TNBS group, DATS prevention group, DATS gastric infusion group, DATS enteral infusion group, dexamethasone group, sulfasalazine group and balsalazide sodium group. Colitis model was established by infusion enema with 50% ethanol containing 150 mg/kg TNBS. All the rats were sacrificed 2 weeks later, macroscopic score and pathologic score were assessed. The serum levels of TNF-ct, IL-113, IL-IO and IL-4 were determined by ELISA. Expression of NF-KB in intestinal mucosa was detected by Western blotting. Results： Compared with control group, macroscopic score and pathologic score in TNBS group were significantly increased （ P 〈 0.05 ）, weight was significantly decreased （ P 〈 0.05 ）, serum levels of TNF-α and IL-1β were significantly increased （P 〈 0.05 ）, serum levels of IL-4 and IL-10 were significantly decreased （ P 〈 0.05 ）, and expression of NF-KB was significantly increased （ P 〈 0. 05 ）. When DATS was used for prevention or treatment of TNBS-induced colitis, all the above-mentioned indices significantly improved （ P 〈 0. 05 ）, however, efficacy of DATS prevention or treatment was inferior to dexamethasone, sulfasalazine and balsalazide sodium. Conclusions： DATS plays a protective role in TNBS-induced colitis in rats, probably via the regulation of cytokines and NF-κB.
出处
《胃肠病学》
2012年第7期394-398,共5页
Chinese Journal of Gastroenterology
