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作 者:齐胤良[1] 桂淑玉[1] 王勇生[2] 张素梅[3] 何苇[3] 周青[3] 汪渊[3]
机构地区:[1]安徽医科大学第一附属医院呼吸内科,合肥230022 [2]巢湖市第一人民医院呼吸内科,巢湖238000 [3]安徽医科大学分子生物学实验室,合肥230032
出 处:《安徽医科大学学报》2010年第1期9-12,共4页Acta Universitatis Medicinalis Anhui
基 金:安徽省自然科学基金资助项目(编号:090413116)
摘 要:目的研究哮喘大鼠模型支气管肺组织骨桥蛋白(OPN)表达变化及其调控机制;探讨地塞米松(DXM)对哮喘大鼠模型支气管肺OPN表达的影响及其机制。方法SD大鼠24只,随机分为正常对照组(A组)、哮喘模型组(B组)、DXM治疗组(C组)。以卵蛋白(OVA)致敏和激发建立大鼠支气管哮喘模型,肺组织切片用于HE染色以观察支气管组织学变化;用免疫组织化学和免疫印迹法分析三组大鼠支气管肺组织中OPN的表达及ERK、p38的磷酸化水平。结果B组大鼠支气管肺组织OPN表达较A组增加,DXM对其表达有明显抑制作用(P<0.05);B组支气管肺组织ERK磷酸化水平较A组明显增加,DXM对其磷酸化有明显抑制作用(P<0.05);而支气管肺组织p38磷酸化水平在B组与A组之间无明显变化,但C组p38磷酸化水平明显下降。结论DXM对OPN表达的增加有抑制作用,其可能的机制是通过ERK信号通路影响OPN的表达。Objective To investigate the expression of osteopontin(OPN)in bronchial lung tissue of asthma rat model and the regulatory mechanism,and the influence of dexamethasone on OPN expression in bronchial lung tissue of asthma rat model.Methods Twenty-four SD rats were randomly divided into control group(group A),asthma model group(group B),DXM group(group C).Asthma rat model was established by sensitization and stimulation with ovalbumin(OVA).Bronchial lung tissue slices were stained with HE to observe the histology changes of bronchus.The expression of bronchial epithelial cell OPN and the phosphorylation levels of ERK,p38 in the three groups were analysed by immunohistochemistry test and Western blot.Results The expression of OPN in bronchial lung tissue of asthma model group was more increased than that in control group and DXM had an obvious inhibition effect on the expression of OPN(P〈0.05).The phosphorylation level of ERK in bronchial lung tissue of asthma model group was more significantly increased than that in control group and DXM had an obvious inhibition effect on the phosphorylation levels(P〉0.05).The phosphorylation levels of p38 did not change in asthma model group and control group,but the phosphorylation levels of p38 in DXM group was obviously decreased.Conlusion OPN expression significantly increase in bronchial lung tissue of asthma group.Dexamethasone has an obvious inhibition effect on the expression of OPN in bronchial lung tissue of asthma model group,which is probably regulated by ERK pathway.
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