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作 者:陆韦[1] 王蕾[1] 谯明[1] 王玉[2] 江吉富[2] 吴中明[2]
机构地区:[1]遵义医学院附属医院儿科,遵义563099 [2]遵义医学院微免教研室,遵义563003
出 处:《医药导报》2014年第8期997-1000,共4页Herald of Medicine
基 金:贵州省科技厅基金资助项目(黔科合J字LKZ[2010]14号)
摘 要:目的通过检测支气管肺泡灌洗液(BALF)中白细胞介素-25(IL-25)和γ-干扰素(IFN-γ)的水平,探讨地塞米松对小鼠支气管哮喘的治疗作用机制。方法清洁级Balb/c小鼠随机分为正常对照组、哮喘组和地塞米松组。以鸡卵清蛋白(OVA)致敏激发法建立哮喘小鼠模型。地塞米松组在每次激发前1 h予地塞米松腹腔注射。每次激发时观察小鼠的表现。于末次激发24 h处死小鼠,取右肺作苏木精-伊红(HE)染色病理切片,显微镜下观察炎症情况;收集左肺BALF,镜下计数白细胞总数、嗜酸性粒细胞(EOS)绝对数目,计算EOS百分比;用酶联免疫吸附法(ELISA)测定BALF中IL-25和IFN-γ的水平,并做相关性分析。结果哮喘组小鼠BALF中白细胞总数、EOS数目和百分比分别与正常对照组、地塞米松组比较均明显增加(P<0.05),而以上3个指标在正常对照组和地塞米松组间差异无统计学意义。哮喘组小鼠BALF中IL-25水平高于正常对照组和地塞米松组(P<0.05),而地塞米松组的含量也高于正常对照组;IFN-γ水平低于正常对照组和地塞米松组(P<0.05),而后两组差异无统计学意义。各组小鼠BALF中IL-25和IFN-γ水平都呈负相关。结论地塞米松治疗哮喘病的部分机制是减轻肺部炎症和促进IFN-γ的产生,同时可能抑制IL-25的表达。Objective To investigate the mechanism of therapeutic action of dexamethasone on asthmatic mice by detecting the levels of IL-25 and IFN-γ in bronchoalveolar lavage fluid (BALF). Methods Balb/c mice with SPF grade were randomly divided into normal control group, asthma group and dexamethasone group. Asthma group and dexamethasone group were sensitized and challenged with ovalbumin ( OVA) . Dexamethasone group was intraperitoneally injected with dexamethasone one hour before challenging. The mice were executed 24 hours after the last challenge, and the HE stained pathological sections of the right lung were made. Pathological sections of lung were observed. BALF in the left lung was also collected. The total white blood cell count and absolute eosinophile ( EOS) count were observed, and the percentage of EOS was calculated. The levels of IL-25 and IFN-γwere measured with ELISA, and correlation analyses were made. Results The counts of total white blood cell and EOS, and the percentage of EOS were significantly higher in the asthma group than in the normal control group and dexamethasone group (P〈0. 05). No differences were found between the normal control group and dexamethasone group. The IL-25 level was higher in the asthma group than in the normal control group and dexamethasone group (P〈0. 05), and its level in the dexamethasone group was also higher than that in the normal control group. The IFN-γlevel was lower in the asthma group than in the normal control group and dexamethasone group (P〈0. 05), while there was no significant difference between the normal control group and dexamethasone group. IL-25 was negatively correlated with IFN-γin each group. Conclusion Part of the mechanisms of dexamethasone acting on asthma are related to its inhibition on the pulmonary inflammation and promotion on the expression of IFN-γ, and possible inhibition of IL-25 expression.
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