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作 者:李艳华[1] 王美怡[1] 金蓉[1] 郭盛[1] 范小勇[2] 马辉[2] 吴良霞[1] 张建华[1]
机构地区:[1]上海交通大学附属第六人民医院儿科,上海200233 [2]复旦大学附属公共卫生临床中心科学研究部,上海202508
出 处:《中国当代儿科杂志》2012年第5期371-374,共4页Chinese Journal of Contemporary Pediatrics
摘 要:目的穿心莲内酯是中药穿心莲的主要有效成分,在体内外均具有较强的抗炎作用。该研究观察穿心莲内酯对哮喘小鼠支气管肺泡灌洗液(BALF)中嗜酸性粒细胞、eotaxin及IL-5表达的影响。方法 32只BALB/c小鼠随机分为对照组、哮喘组、布地奈德组、穿心莲内酯组,每组8只。以卵清蛋白(OVA)致敏激发建立哮喘小鼠模型。ELISA法检测BALF及外周血中eotaxin、IL-5的水平,实时荧光定量PCR法检测肺组织eotaxin、IL-5mRNA的表达。结果穿心莲内酯明显抑制哮喘小鼠BALF中嗜酸性粒细胞(P<0.05)浸润,且作用强于布地奈德(P<0.05);与哮喘组相比,穿心莲内酯组小鼠BALF中eotaxin、IL-5,肺组织中eotaxin mRNA和外周血中IL-5的表达明显降低(P<0.05),但仍高于布地奈德组(P<0.05);同时穿心莲内酯抑制哮喘小鼠外周血中eotaxin和肺组织IL-5 mRNA的表达(P<0.05),作用与布地奈德比较差异无统计学意义(P>0.05)。结论穿心莲内酯通过降低哮喘小鼠eotaxin、IL-5的表达,抑制哮喘气道嗜酸性粒细胞浸润。Objective Andrographolide, the active component in andrographis paniculata, has potent anti- inflammatory actions. This study aimed to evaluate the effects of andrographolide on eosinophil granulocytes (EOS) and the expression of eotaxin and IL-5 in mice with asthma. Methods BALB/c mice were randomly assigned into normal control, asthma, budesonide treatment and andrographolide treatment groups (n = 8 each). Mice in the latter three groups were sensitized and challenged with ovalbumin (OVA) to induce asthma. ELISA was used to detect the concentrations of eotaxin and IL-5 in bronchoalveolar lavage fluid (BALF) and peripheral blood. The expression of eotaxin mRNA and IL-5 mRNA in lung tissues was detected by real-time quantitative PCR. Results Andrographolide treatment significantly decreased EOS count in BALF (P 〈 0. 05 ) and the effect of andrographolide was better than the effect of budesonide. Andrographolide treatment significantly down-regulated the expression of eotaxin and IL-5 in BALF, lung eotaxin mRNA expression and blood IL-5 expression ( P 〈 0.05 ), but the effects of andrographolide were poorer than the effects of budesonide. Andrographolide treatment resulted in a decrease in blood eotaxin expression and lung IL-5 mRNA expression and the effects of andrographolide were similar to budesonide. Conclusions Andrographolide can down-regnlate the expression of IL-5 and eotaxin and thus suppress the inflitration of EOS in a mouse model of asthma.
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