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作 者:吕婧[1] 忽新刚[1] 黎镇赐[1] 于霖[1] 丁宁[1] 许立新[1] 佘守章[1]
机构地区:[1]广州医学院附属广州市第一人民医院,510000
出 处:《实用医学杂志》2011年第22期4037-4039,共3页The Journal of Practical Medicine
基 金:广州市医药卫生科技重点资助项目(编号:2009-ZDi-02)
摘 要:目的:研究肾上腺素α_2受体调控的炎症信号传导MAPK通路对呼吸机所致肺损伤大鼠肺部炎症反应的影响。方法:30只SPF级雄性SD大鼠随机均分成5组:常规潮气量通气组(C,8 mL/kg,呼吸频率90次/min),大潮气量通气组(H,20 mL/kg,呼吸频率50次/min),大潮气量通气盐酸右旋美托咪啶处理组(D,参数设置同H组),大潮气量通气育亨宾处理组(Y,参数设置同H组),大潮气量通气+盐酸右旋美托咪啶+育亨宾处理组(D+Y,参数设置同H组)。观察肺部病理改变,ELISA法检测支气管肺泡灌洗液(BALF)中的肿瘤坏死因子α、IL-1β、IL-6和IL-10,Western Blot方法检测各组肺组织中促分裂原活化蛋白激酶及其和磷酸化水平。结果:和C组相比,H组、D组、Y组和D+Y组大鼠肺组织病理改变,BALF中的TNF-α、IL-1β、IL-6、IL-10和MIP-2,以及肺部磷酸化ERK1/2均有明显增高。H组、Y组和D+Y组相比,D组肺组织和BALF中各项指标均显著降低。结论:α_2受体激动剂能通过调控MAPK通路显著减轻VILI所造成的肺部炎症反应,提示α_2受体在VILI所造成的肺部炎症反应中起到重要作用。Objective To elucidate the effect of alpha-2 adrenoceptor-regulated inflammatory signal pathway MAPK on the lung inflammatory response in a rat model of ventilator-induced lung injury. Methods Thirty SPF adult male Sprague-Dawley rats were randomly divided into five groups (n = 6 per group) : standard ventilation group (C), high-tidal volume ventilation group (H), high-tidal volume ventilation plus dexmedetomidine (D), high-tidal volume ventilation plus yohimbine(Y), high-tidal volume ventilation plus dexmedetomidine and yohimbine (D+Y).The pulmonary pathologic changes were observed. The levels of tumor necrosis factor α, interleukin (IL-1 1β, IL-6 and IL-10) in the BALF were determined by ELISA assay. The expressions of ERKI/2 and p-ERK1/2 were measured by Western blot method. Results Compared with Group C, Group H, D, Y, and D+Y had a significant pulmonary pathologic changes (P 〈 0.01). The expression levels of TNF-α, IL-1β, IL-6 and IL-10 in BALF in Group H, D, Y and D+Y were significantly higher than those in Group C. The indices of lung tissue homogenization and BALF in Group D were significantly lower than those in Group H,D,Y,and D+Y. Conclusion Alpha-2 adrenoceptor agonist significantly attenuated the inflammation response of lung underwent injurious ventilation via regulating the MAPK pathway, indicating that alpha-2 adrenoceptor plays an important role in the pulmonary inflammation of VILI.
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