雷公藤内酯醇抑制次级淋巴组织趋化因子表达对小鼠实验性结肠炎的影响  

Influence of inhibiting expression of SLC by triptolide on experimental ulcerative colitis in mice

作　　者：张霞[1] 周国雄[2] 张海峰[2] 陈海琴[2] 曹维[2] 

机构地区：[1]大丰市人民医院消化内科,江苏省大丰市224100 [2]南通大学附属医院消化内科,江苏省南通市226001

出　　处：《世界华人消化杂志》2014年第20期2893-2899,共7页World Chinese Journal of Digestology

基　　金：南通市应用研究汁划基金资助项目;No.BK2012074;南通大学自然科学基金资助项目;No.10Z061~~

摘　　要：目的:研究实验性结肠炎小鼠中次级淋巴组织趋化因子(secondary lymphoid tissue chemokine,SLC)的表达,了解不同浓度雷公藤内酯醇(triptolide,TL)抑制SLC表达对小鼠结肠炎的影响.方法:40只♀Balb/c小鼠随机分为5组:正常组、葡聚糖硫酸钠(dextran sodium sulphate,DSS)模型组、丙二醇治疗组、TL治疗组1、TL治疗组2.正常组小鼠饮用蒸馏水,其余小鼠饮用5%DSS溶液7 d,诱导建立实验性结肠炎模型以模拟人类溃疡性结肠炎(ulcerative colitis,UC).治疗组从造模第3天开始,丙二醇治疗组给予2%丙二醇0.2 mL腹腔注射(ip),TL治疗组分别给予溶于2%丙二醇的TL 0.6 mg/kg、TL 0.8 mg/kg,qd,ip 5 d.第8天处死小鼠后检测结肠长度、结肠大体形态评分、结肠组织学病理评分,应用免疫组织化学、实时荧光定量PCR检测小鼠结肠组织中SLC表达.结果:SLC在小鼠正常组中微弱表达,在小鼠UC中表达上调,正常组与DSS组、丙二醇治疗组相比差异有统计学意义(P<0.01);丙二醇治疗组小鼠与DSS组相比,SLC表达无明显差异(P>0.05);TL治疗组小鼠症状减轻,SLC表达下调,与DSS组、丙二醇治疗组相比,差异有统计学意义(P<0.01).结论:SLC表达参与了UC的发生和发展,TL对小鼠实验性结肠炎的治疗效应与抑制SLC的表达有相关性.AIM： To explore the influence of inhibiting theexpression of secondary lymphoid tissue chemokine（SLC） by triptolide（TL） on experimentalcolitis in mice. METHODS： Forty female Balb/c mice were randomly divided into five groups： a normal group,a model group, a propanediol treatment group, a low-dose TL treatment group, and a high-dose TL treatment group. Mice in the normal group were given distilled water, while the other groups were given 5% dextran sodium sulphate solution for 7 d to induce colitis mimicking human ulcerative colitis（UC）. From the 3^rd day of colitis induction, the propanediol treatment group was given 2% propanediol（0.2 mL） daily by intraperitoneal injection, while the TL treatment groups were given TL 0.6 and 0.8 mg/kg, respectively, for 5 d. All the mice were killed on day 8. Colon length, colon gross morphology score and colon histological score were assessed. The expressions of SLC in colon tissue was measured by immunohistochemistry and real-time fluorescence quantitative PCR. RESULTS： SLC was expressed weakly in the normal group, and was up-regulated in colitis. SLC expression in the normal group was significantly lower than that in the model group and propanediol treatment group（P〈0.01）, although there was no significant difference between the latter two groups（P〉0.05）. The expression of SLC in the TL treatment groups was lower than that in the model group and propanediol treatment group（P〈0.01）, and the pathological changes were mitigated. CONCLUSION： The expression of SLC may be related to the occurrence and development of UC. The therapeutic effect of TL against experimental ulcerative colitis in mice may be associated with restraining the expression of SLC.

关 键 词：溃疡性结肠炎 次级淋巴组织趋化因子 雷公藤内酯醇 

分 类 号：R574.62[医药卫生—消化系统]