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作 者:郑秦[1] 管宇[1] 王志成[2] 王健英[3] 浦益琼[3] 王国华[1] 张晓峰[1] 夏菁[1] 崔乐乐[4] 罗梅宏[4]
机构地区:[1]上海中医药大学附属上海市中医医院 [2]复旦大学附属华山医院 [3]上海中医药大学药学院 [4]上海中医药大学附属曙光医院宝山分院
出 处:《中医杂志》2015年第20期1767-1770,共4页Journal of Traditional Chinese Medicine
基 金:国家自然科学基金(81102569);上海市卫生和计划生育委员会科研项目(201440587)
摘 要:目的探讨异功散对炎症诱发的铁代谢紊乱的影响。方法 40只C57BL/6小鼠随机分为空白对照组、异功散组、脂多糖组、异功散加脂多糖组,每组10只。异功散组、异功散加脂多糖组给予异功散灌胃10.57 g/(kg·d),空白对照组每只灌胃0.2 ml超纯水,各组均连续灌胃7天。第8天,脂多糖组和异功散加脂多糖组腹腔注射脂多糖1.5 mg/kg建立铁代谢紊乱模型,6h后处死所有小鼠。检测血常规、血清铁和肝组织铁含量、血清和肝组织白细胞介素6(IL-6)含量。结果各组小鼠血常规无明显变化,差异无统计学意义(P>0.05)。与空白对照组比较,脂多糖组小鼠血清铁降低,肝组织铁和血清、肝组织IL-6均明显上升(P<0.05),而异功散组加脂多糖组较脂多糖组肝组织铁、血清和肝组织IL-6均明显下降(P<0.05)。结论异功散可改善脂多糖介导的急性炎症条件下的铁代谢紊乱,其机制可能与降低血清和肝组织IL-6有关。Objective To explore the impact of Yigong Powder on iron metabolism disorder induced by inflammation. Methods 40 C57 BL /6 mice were randomly divided into control group( n = 10),Yigong Powder group( n = 10),lipopolysaccharide group( n = 10) and Yigong Powder combined with lipopolysaccharide group( n = 10).Yigong Powder group and Yigong Powder combined with lipopolysaccharide group were given 10. 57 g /( kg ·d) of Yigong Powder by gavage. Control group was given 0. 2 ml of ultrapure water,all for seven days. On the eighth day,lipopolysaccharide group and Yigong Powder combined with lipopolysaccharide group were given 1. 5 mg / kg of lipopolysaccharide by intraperitoneal injection to establish iron metabolism disorder models. Six hours later,all mice were sacrificed. Blood routine,serum levels of iron and interleukin 6( IL-6),and content of iron and IL-6 in liver tissue were detected. Results Blood routine changed little in every group( P〉0. 05). Compared with control group,serum level of iron decreased,serum level of IL-6,as well as content of iron and IL-6 in liver tissue increased in lipopolysaccharide group( P〈0. 05). Compared with lipopolysaccharide group,iron content in liver tissue,as well as IL-6 in serum and liver tissue decreased in Yigong Powder combined with lipopolysaccharide group( P〈0. 05).Conclusion Yigong Powder could improve iron metabolism disorder mediated by lipopolysaccharide under acute inflammation. The mechanism may relate to decrease of IL-6 in serum and liver tissue.
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