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作 者:毕洪钟 潘金[1] 王伟[1] 段才华[1] 周湘明[1] 琚坚[1]
机构地区:[1]昆明医科大学第二附属医院特需病房,云南昆明650101
出 处:《胃肠病学和肝病学杂志》2015年第3期305-308,共4页Chinese Journal of Gastroenterology and Hepatology
基 金:云南省卫生科技计划项目(2011WS0096)
摘 要:目的研究DNAM-1在CCL4诱导肝纤维化大鼠肝组织中的表达情况,以及阴行草水煎液对其干预作用。方法 120只健康SD大鼠随机分为6组:空白对照组、模型组、阴行草组、丹参组、虎杖组及易善复组,每组20只。CCL4皮下注射诱导大鼠肝纤维化模型。同时,空白对照组、模型组予生理盐水灌胃,其余4组大鼠分别予阴行草、丹参、虎杖水煎液及易善复灌胃干预。10周后处死大鼠,光镜下观察其肝脏病理组织学改变,进行肝纤维化分期。利用免疫组化SP法检测各组大鼠肝组织中DNAM-1表达水平,应用计算机图像分析技术对免疫组化结果进行定量分析。结果与模型组相比,阴行草组可明显降低CCL4诱导的肝纤维化程度(P<0.05);阴行草组大鼠肝组织中DNAM-1高于空白对照组,低于模型组(P<0.01)。结论 DNAM-1在肝纤维化大鼠肝脏组织中过表达;阴行草水煎液对CCL4诱导肝纤维化大鼠肝纤维化有明显的防治作用,其主要机制可能是抑制了DNAM-1的表达。Objective To investigate the expression of DNAM-1 in rats with liver fibrosis by carbon tetrachloride (CCIA) , meanwhile research the Siphonostegia chinensis decoction intervention. Methods One hundred and twenty healthy SD rats were randomly divided into six groups: blank control group, model group, Siphonostegia chinensis group, Salvia miltiorrhiza group, Polygonum cuspidatum group and Phosphatidylcholine Capsules group. The model of liver fibrosis was induced by subcutaneous injection with CCL4. At the same time, the rats in the blank control group and model group were gavaged with physiological water; rats in Siphonostegia chinensis group, Salvia mihiorrhiza group, Polyonum cuspidatum group and phosphatidylch oline capsules group were given by Siphonostegia chinensis decoction, Salvia mihiorrhiza decoction and Polyene Phosphatidylcholine Capsules respectively. After 10 weeks, all rats were exe- cuted. DNAM-1 in the liver was examined by SP, the results were analyzed by computer image analysis technique. Re- suits Compared with model group, the degree of liver fibrosis was reduced in Siphonostegia chinensis grup (P 〈 0.05). The expression of DNAM-1 in Siphonostegia chinensis group was higher than that in the blank control group, lower than that in the model group (P 〈 0.01 ). Conclusion DNAM-1 can express in rats with liver fibrosis. The pro- tective effect of Siphonostegia chinensis decoction has been confirmed in liver fibrosis rats induced by CCIA. The main mechanism may inhibit the expression of DNAM-1.
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