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作 者:迟宏罡[1] 郑学宝[1] 赵兵[1] 李文洋[1] 万郑 戴世学[3] 冯锦山[1] 于丰彦[1] 邹颖[1,2]
机构地区:[1]广东医学院第二临床医学院中医学教研室,东莞523808 [2]广东医学院中美肿瘤研究所,东莞523808 [3]南方医科大学南方医医院,广州510515
出 处:《中华中医药杂志》2015年第2期565-568,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金资助项目(No.81173240);广东医学院博士启动项目(No.2013005;No.2013006)~~
摘 要:目的:探讨黄芩汤对葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠结肠黏膜NF-κB p65的影响。方法:用DSS诱导结肠炎小鼠模型,实验设对照组、DSS组、DSS+黄芩汤组(130mg/kg)、DSS+美沙拉嗪组(7.4mg/kg),每组8只;3.5%DSS自由饮用7d制成结肠炎小鼠模型后第2天进行治疗,连续7d。观察小鼠体质量变化和结肠病理组织评分,异硫氰酸荧光素葡聚糖灌胃检测肠道通透性,Western blot法检测小鼠结肠组织NF-κB p65蛋白表达水平。结果:与模型组比较,黄芩汤能增加DSS诱导的结肠炎小鼠体质量(P<0.01),降低结肠病理组织评分(P<0.05),对肠道上皮屏障功能具有保护作用,降低结肠组织中NF-κB p65蛋白表达水平(P<0.01)。结论:黄芩汤能够对DSS诱导的结肠炎小鼠模型起到保护作用,其作用机制可能与保护肠道上皮屏障功能、抑制NF-κB p65活化有关。Objective: To explore the intervention effect of Huangqin decoction on NF-κB p65 in mice with colonitis induced by dextran sulfate sodium(DSS). Methods: C57BL/6 mice were equally and randomly divided into normal control group, model group, DSS plus Huangqin Decoction group(130mg/kg) and DSS plus mesalazine group(7.4mg/kg), 8 mice in each group. Mice in model group, DSS plus Huangqin Decoction group and DSS plus mesalazine group were given water containing 3.5% DSS to drink freely to establish the colitis mice model. The mice in the treatment group were treated with corresponding drugs on the 2nd day after model establishment. Body weight changes and histopathological score were observed. Intestinal permeability was tested by the method of FITC-dextran lavage. Western blot was used to test NF-κB p65 expression in colon of mice. Results: Compared with the model group, Huangqin Decoction could increase the weight of mice with colonitis induced by DSS(P〈0.01), decrease the histopathological score(P〈0.05), protect the barrier function of intestinal epithelial, and decrease the expression level of NF-κB p65 in colon of mice(P〈0.01). Conclusion: Huangqin Decoction could protect the mice with colonitis induced by DSS, and the mechanism might be related to the protection of intestinal epithelial barrier function and inhibition of NF-κB p65 activation.
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