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作 者:王燕 冯大鹏[2] 孙连碧 张宝辉[3] WANG Yan;FENG Da-peng;SUN Lian-bi;ZHANG Bao-hui(Department of Medical Service Teaching and Research, Medical Service Training Team of Joint Logistics Support Force, Dalian116017;department of orthopedics, Second Affiliated Hospital of Dalian Medical University, Dalian 116027;Deptment of Neurobiology, Basic Medical College, China Medical University, Shenyang 110122, China)
机构地区:[1]联勤保障部队综合训练大队卫勤训练队卫勤教研室,辽宁大连116017 [2]大连医科大学附属第二医院骨科,辽宁大连116027 [3]中国医科大学神经生物学教研室,辽宁沈阳110001
出 处:《解剖科学进展》2019年第4期450-452,456,共4页Progress of Anatomical Sciences
基 金:国家自然科学基金(81070011)
摘 要:目的探讨促红细胞生成素对哮喘小鼠肺组织血管内皮生长因子(VEGF)及细胞间黏附分子(ICAM)-1的影响。方法36只BALB/c小鼠,雌雄不限,随机分为对照组、哮喘组和促红细胞生成素组,卵蛋白致敏的方法制备哮喘小鼠模型。用乙酰甲胆碱行支气管激发试验,测定各组小鼠气道阻力的变化;收集支气管肺泡灌洗液(BALF),进行细胞总数计数及嗜酸性粒细胞计数,免疫组织化学和Westernblot方法检测各组小鼠肺组织VEGF与ICAM-1的表达。结果促红细胞生成素能够降低哮喘小鼠的气道阻力,降低BALF中细胞总数及嗜酸粒细胞数(P<0.01)。免疫组织化学和Westernblot的光密度值分析结果显示,促红细胞生成素组小鼠肺组织VEGF与ICAM-1蛋白表达的平均光密度值显著低于哮喘组小鼠(P<0.01)。结论促红细胞生成素可降低哮喘小鼠气道阻力及肺内炎症,与下调VEGF与ICAM-1的蛋白表达相关。Objective To investigate the effects of erythropoietin on vascular endothelial growth factor(VEGF) and intercellular adhesion molecule(ICAM)-1 in lung tissue of asthmatic mice. Methods 36 BALB/c mice, with no sex limitation, were randomly divided into control group, asthma group and erythropoietin group. Changes of airway resistance in mice were measured by bronchial provocation test with methacholine. Bronchoalveolar lavage fluid(BALF) was collected to count the total number of cells and eosinophils. The expressions of VEGF and ICAM-1 in lung tissue of mice were detected by immunohistochemistry and Western blot. Results Erythropoietin reduced the airway resistance, the number of total cells and eosinophil in BALF of asthmatic mice(P<0.01). Immunohistochemistry and Western blot showed that the expression levels of VEGF and ICAM-1 in lung tissue of mice was significantly lower in erythropoietin group than in asthma group(P<0.01). Conclusion Erythropoietin reduces airway resistance and pulmonary inflammation in asthmatic mice, which is related to down-regulation of the expression of VEGF and ICAM-1 proteins.
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