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作 者:刘世昌[1] 张铁军[1] 邓毅书 陆地[1] 詹东[1] 李跃敏[1]
机构地区:[1]昆明医科大学人体解剖与组织胚胎学教研室,云南昆明6505002 [2]云南省第三人民医院呼吸内科,云南昆明650011
出 处:《昆明医科大学学报》2013年第6期21-25,45,共6页Journal of Kunming Medical University
基 金:云南省应用基础研究计划面上项目(2008CD207);昆明医科大学硕士研究生创新基金资助项目(2012J19)
摘 要:目的研究白藜芦醇对SD大鼠慢性阻塞性肺疾病(COPD)的抗氧化作用及其机制.方法对照组采用蒸馏水雾化吸入120 d,模型组采用丙烯醛(acrolein)6.87μg/L雾化吸入120 d,预防组分为白藜芦醇(resveratro)l低剂量5 mg/(kg.d)、中剂量15 mg/(kg.d)、高剂量45 mg/(kg.d)灌胃给药1 h后采用丙烯醛雾化吸入120d.检测肺功能指标:肺顺应性(CL)、第0.3秒用力呼气容积(FEV0.3)/用力肺活量(FVC)、呼气流量峰值(PEF)、最大呼气中段流量(MMF),用ELISA法测定支气管肺泡灌洗液(BALF)中前列腺素E2(PGE2)含量,运用逆转录PCR检测大鼠肺组织中环氧合酶-2(COX-2)、核转录因子-κB/p65(NF-κB/p65)mRNA表达量的变化,运用Western Blotting检测大鼠肺组织中p38促分裂原活化蛋白激酶(p38 mitogen-activated protein kinases,p38 MAPK)通路蛋白的表达及其变化规律.结果白藜芦醇能增加大鼠COPD的CL、FEV 0.3/FVC、PEF和MMF,降低BALF中PGE2的含量,减少大鼠肺组织中COX-2、NF-κB/p65 mRNA的表达并呈剂量依赖性,降低大鼠肺组织中p38 MAPK的磷酸化.结论白藜芦醇对大鼠COPD具有干预作用,其作用机制可能与下调p38MAPK的磷酸化水平从而抑制炎症蛋白酶的释放有关.Objective The study was purposed to investigate the antioxidation and its mechanism of resveratrol in the acrolein-stimulated rats with chronic obstructive pulmonary disease (COPD) . Methods During the experiments, rats were randomly divided into five groups, including the blank control group, the acrolein-stimulated group (6.87 Ix g/L) and three 5, 15 and 45 mg/Kg.d for 1 h, respectively) prevention groups (acrolein treatment after giving resveratrol at . Pulmonary function indicators were detected including lung compliance (CL), 0.3 seconds forced expiratory volume (FEV0.3) /forced vital capacity (FVC), peak expiratory flow (PEF) and maximal mid-expiratory flow (MMF) . The content of prostaglandin E2 (PGE2) was measured by Griess reagent and ELISA. The mRNA and protein levels of proinflammatory enzymes cyclooxygenase-2 (COX-2) and nuclear transcription factor-K B /p65 (NF-s: B /p65) were analyzed by RT-PCR. And the phosphorylation levels of p38 MAPK was measured by western blotting. Results Compared with the model group, the level of CL and the ratio of FEVO.3/FVC were increased significantly after treatment with resveratrol. Resveratrol
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