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作 者:姚迪翡[1,2] 徐翔[1] 陈中婷[1] 武良琴 潘文胜[1]
机构地区:[1]浙江大学医学院附属第二医院,杭州310009 [2]浙江大学药学院,杭州310058 [3]安徽省第二人民医院,合肥230000
出 处:《中国药学杂志》2013年第24期2117-2122,共6页Chinese Pharmaceutical Journal
基 金:国家卫生部公益性行业专项基金(200802112);浙江省卫生厅科研计划(2008A094);浙江省自然科学基金资助项目(Y2080001);浙江省中医药管理局重大项目(2008ZA011);浙江省科技厅重大项目(2009C03012-5)
摘 要:目的研究地衣芽孢杆菌对小鼠溃疡性结肠炎的治疗作用和可能机制。方法 BABL/c小鼠,随机分为8组各8只。评价记录小鼠的一般情况,HE染色观察小鼠肠黏膜组织学改变,免疫组化检测小鼠结肠黏膜NF-κB和Bcl-2的表达情况。结果与造模组、溶剂组相比,各治疗组小鼠一般情况较好;结肠大体损伤评分和组织病理学改变评分均较低;结肠黏膜NF-κB和Bcl-2的表达均明显降低,且差异均有统计学意义(P<0.05)。地衣芽孢杆菌联合用药组与地衣芽孢杆菌单独用药组相比,结肠大体损伤评分、组织病理学改变评分、NF-κB、Bcl-2表达均较低,差异亦具有统计学意义(P<0.05)。结论地衣芽孢杆菌对DSS诱导的小鼠溃疡性结肠炎具治疗作用,且与柳氮磺胺吡啶联合给药时治疗作用更明显;且该作用可能是通过抑制结肠黏膜NF-κB和Bcl-2蛋白的表达而实现。OBJECTIVE To investigate the therapeutic efficacy of treatment of Bacillus licheniformis (BL) on ulcerative colitis (UC) in BALB/c mice. METHODS The therapeutic effect of different treatment was evaluated in seven acute UC mice groups and one control group, including the normal group, the model group, the solvent group, the sulfasalazine (SASP) treated group, the high dose BL treated group, the low dose BL treated group, the high dose BL with SASP treated group and the low dose BL with SASP trea- ted group. The disease activity index (DAI) score of mice were recorded every other day since the experiment started. On the 15th day, all the mice were killed, then gross injury score in colonic mueosa and histopathological changes were measured. The expression levels of NF-κB and Bcl-2 in mouse colonic mucosa was also determined by immunohistochemistry method. RESULTS The DAI score, the colonic gross injury score, the histopathological changes and the expression level of NF-κB and Bcl-2 of mice colonic mucosa in drug treated groups were decreased significantly when comparing with the drug untreated groups. Moreover, these results were even better in two drugs combined treated groups than in single drug treated groups ( P 〈 0. 05 ). CONCLUSION BL has the efficacy of remission DSS-induced acute ulcerative colitis in mice, and there is more effective when it is administered with SASP. The results indi- cat that the therapeutic effort is via inhibiting the expression of NF-κB and Bcl-2 in colonic mucosa.
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