黄蜀葵花提取物对小鼠IBD的治疗作用及TNF-α、IFN-γ表达的影响

Effects of Abelmoschi Corolla Extracts on IBD Treatment in Mice and Expression of TNF-α and IFN-γ

目的探讨黄蜀葵花提取物对炎症性肠病(IBD)的治疗作用及其可能机制。方法 BABL/c小鼠80只,随机分为正常对照组、模型组、柳氮磺吡啶组和黄葵提取物组,每组20只,后3组用TNBS诱导建立小鼠IBD模型。造模开始时,柳氮磺吡啶组和黄葵提取物组分别给予0.5g/kg柳氮磺吡啶,3.75g/kg黄蜀葵花提取物灌胃,每日1次,连续28d。实验终点时分析实验动物的存活率、结肠质量长度比值、结肠组织病理变化,以及结肠组织中细胞因子TNF-α和IFN-γ含量。结果正常对照组、模型组、柳氮磺吡啶组和黄葵提取物组动物存活率分别为100%、40%、60%和75%,黄葵提取物组小鼠存活率显著增高,与模型组相比差异有统计学显著意义(P<0.05)。与模型组相比,黄葵提取物组结肠质量长度比值显著降低,差异有统计学意义(P<0.01);结肠组织炎症和隐窝损害显著减轻,病理评分亦显著降低,差异有统计学意义(P<0.01);结肠组织TNF-、IFN-γ含量明显降低,差异有统计学意义(P<0.01)。结论黄蜀葵花提取物能够抑制IBD模型小鼠肠道炎症,提高模型动物生存率,抑制TNF-α和IFN-γ等炎症因子表达可能是其作用机制之一。

OBJECTIVE To investigate the therapeutic effect of Abelmoschi corolla extracts （ACE） on inflammatory bowel disease （IBD） and its possible mechanism. METHODS 80 BABL/c mice were randomly divided into the control group, model group, sulfasalazine group and ACE group, 20 mice in each group. IBD models were established by the induction of TNBS in all groups, except the normal control group. Then, sulfasalazine group and ACE group were administered with 0.5 g/kg sul fasalazine and 3.75 g/kg Abelmoschi corolla extracts respectively, by oral gavage once a day for 28 d. The animal survival rates, the colon weight/length ratios, the tissue Pathology of colon, and the contents of tumor necrosis factor （TNF-α） and 7 -interferon （IFN-γ） in colon tissue were analyzed at the end of experiments. RESULTS The animal survival rates of normal control group, model group, sulfasalazine group and ACE group were 100%, 40%, 60% and 75% respectively. Compared to the model group, the survival rates of mice in ACE group increased significantly, the colon weight/length ratios decreased , pathological scores with notable alleviation of microscopic signs reduced and the contents of cytokines TNF-α and IFN-γ in co- lon tissue decreased, with statistically significant differences （P〈0.05-0.01）. CONCLUSION Abelmoschi corolla extracts can attenuate intestinal inflammation in IBD mice models and improve the animal survival rates. One of the mechanisms is pos- sibly associated with the inhibition of TNF-α, IFN-γ and other inflammatory cytokines.