姜黄素对DSS诱导的小鼠溃疡性结肠炎的疗效  

Eff icacy of curcumin in the management of dextran sulphate sodium-induced ulcerative colitis in mice

作　　者：陈欧[1] 李昌平[1] 罗彬[1] 冯琦[2] 马春华[2] 冯凯祥[2] 

机构地区：[1]四川省泸州医学院附属医院,四川省泸州市646000 [2]四川省绵阳市中心医院,四川省绵阳市621000

出　　处：《世界华人消化杂志》2011年第7期680-686,共7页World Chinese Journal of Digestology

摘　　要：目的:观察姜黄素对葡聚糖硫酸钠(DSS)诱导的小鼠溃疡性结肠炎的疗效,并探讨其作用机制.方法:选♀BALB/c小鼠60只,随机分为4组,每组15只.A组:正常对照组;B组:DSS结肠炎组,小鼠每日自由摄取5%DSS溶液;C组:姜黄素治疗组,小鼠自由摄取5%DSS溶液,每日腹腔注射姜黄素悬液30mg/kg;D组:地塞米松治疗组,饮用5%DSS溶液,每日腹腔注射一次地塞米松针剂0.4mg/kg.各组小鼠每日记录疾病活动指数(DAI)评分,HE染色观察小鼠结肠黏膜组织学改变.ELISA法测定结肠组织中肿瘤坏死因子(TNF)-α、白介素(IL)-6含量.免疫组织化学染色观察核因子-κB(NF-κB)在结肠组织炎性细胞内的表达情况.Western blot检测结肠组织胞质NF-κB抑制蛋白IκB的表达情况.结果:DAI与组织学损伤评分显示C、D组分别与B组比较差异有统计学意义(DAI:1.64±0.92,2.80±0.92vs7.67±1.56;组织学损伤评分:1.36±0.50,2.00±0.67vs2.83±0.83,均P<0.01),C、D组比较差异有统计学意义(P<0.01).TNF-α(ng/L)、IL-6(ng/L)的浓度在B组明显升高,且高于C、D组(TNF-α:102.75±3.52vs75.91±1.59,78.25±2.15;IL-6:80.94±3.26vs59.65±1.39,65.57±4.04,均P<0.01);NF-κB在C、D组中的表达较B组显著下降(2.73±0.79,4.22±1.09vs7.92±1.24,均P<0.01),C、D组之间仍有统计学意义(P<0.05).IκBα在C、D、B组中的表达水平逐渐降低,C、D组和B组比较差异有统计学意义(P<0.05).结论:姜黄素可以有效治疗DSS诱导的小鼠溃疡性结肠炎,其疗效优于地塞米松.其机制可能是通过抑制NF-κB信号通路及调节细胞因子TNF-α、IL-6等的释放而发挥作用.AIM：To investigate the efficacy of curcumin in the treatment of dextran sulphate sodium（DSS）induced ulcerative colitis in mice.METHODS：Sixty female BALB/c mice were randomly divided into four groups：normal group,experimental colitis group（administered with 5% DSS solution）,curcumin treatment group（administered with 5% DSS solution and intraperitoneally injected with curcumin,30 mg/kg body weight）,dexamethasone treatment group（administered with 5% DSS solution and intraperitoneally injected with dexamethasone,0.4 mg/kg body weight）.The severity of colitis was evaluated using the disease activity index（DAI） score,and colonic mucosal histological changes were observed by HE staining.Tumor necrosis factor-α（TNF-α） and interleukin-6（IL-6） levels in colonic tissue were determined by ELISA.The expression of nuclear factor-κB（NF-κB） in intestinal inflammatory cells was determined by immunohistochemistry.The expression of inhibitor of NF-κB（IκB） in intestinal in？ ammatory cells was determined by Western blot.RESULTS：Compared with the normal group and experimental colitis group,treatment with curcumin signif icantly improved symptoms,reduced colonic DAI and histological scores（DAI：1.64 ± 0.92,2.80 ± 0.92 vs 7.67 ± 1.56;histological scores：1.36 ± 0.50,2.00 ± 0.67 vs 2.83 ± 0.83,all P 0.01）,and decreased the levels of colonic TNF-α（ng/L） and IL-6（ng/L）（TNF-α：102.75 ± 3.52 vs 75.91 ± 1.59,78.25 ± 2.15;IL-6：80.94 ± 3.26 vs 59.65 ± 1.39,65.57 ± 4.04,all P 0.01）.Curcumin decreased the expression of NF-κB（2.73 ± 0.79,4.22 ± 1.09 vs 7.92 ± 1.24,both P 0.01） and degradation of IκBα more signif icantly than dexamethasone.CONCLUSION：Curcumin has a positive effect in treating DSS-induced colitis in mice.The therapeutic effect of curcumin is superior to dexamethasone.Curcumin reduces colonic inflammation by decreasing the expression of NFκB and modulating the release of cytokines.

关 键 词：姜黄素 葡聚糖硫酸钠 溃疡性结肠炎 核因子ΚB 

分 类 号：R285.5[医药卫生—中药学]