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作 者:阮琼[1] 苏中昊[2] 杨爱东[2] 李文雯[2] 汪东颖[2] 吴中华[2] 庞慧芳[2]
机构地区:[1]上海市第八人民医院急诊内科,上海200233 [2]上海中医药大学基础医学院,上海201203
出 处:《中国比较医学杂志》2011年第3期39-42,81,共5页Chinese Journal of Comparative Medicine
基 金:上海市教委高校高水平特色发展项目(No.(2005)81);上海高校选拔培养优秀青年教师科研专项基金(P13908)
摘 要:目的探讨内毒素致急性肺损伤(ALI)大鼠肺组织核转录因子-κB(NF-κB)、基质金属蛋白酶2(MMP-2)及其抑制因子(TIMP-2)蛋白和mRNA表达的变化。方法 20只雄性Wistar大鼠随机分为2组:对照组、LPS模型组,每组再分为4 h和8 h两个亚组。尾静脉注射脂多糖(LPS)(10 mg/kg)建立大鼠急性肺损伤模型。检测血白细胞计数、支气管肺泡灌洗液(BALF)蛋白含量,采用免疫组化ABC法和实时荧光定量PCR分别测定肺组织NF-κB、MMP-2、TIMP-2蛋白及其mRNA的表达,并观察肺组织病理变化。结果与对照组相比,模型组4 h和8 h时大鼠肺组织中的NF-κB、MMP-2蛋白染色阳性面积率及其mRNA表达均显著增高(P<0.01)、TIMP-2蛋白染色阳性面积率及其mRNA表达均明显降低(P<0.05或P<0.01)。病理学观察显示,模型组大鼠肺组织出现出血及坏死。结论内毒素致急性肺损伤的发病机制可能与NF-κB、MMP-2蛋白及其mRNA表达升高、TIMP-2蛋白及其mRNA表达降低有关。Objective To investigate the changes of NF-κB,MMP-2 and TIMP-2 protein and its mRNA in the rats with acute lung injury(ALI) caused by lipopolysaccharide(LPS).Methods Twenty male Wistar rats were randomly divided into two groups: normal control group,LPS model group.Each group had two subgroups,4 hours and 8 hours after LPS were injected.The ALI model was established by intravenous injection of LPS(10 mg /kg)through a tailvein.Then the white blood cell(WBC) in blood and the protein content in bronchial alveolar lavage fluid(BALF) were measured,the expressions of nuclear factor-κB(NF-κB),matrix metalloproteinase-2(MMP-2) and tissue inhibitor of matrix metalloproteinases(TIMP-2) protein in pulmonary tissues were measured by immunohistochemistry ABC,the expression NF-κB,MMP-2 and TIMP-2mRNA were measured by real-time fluorescent polymerase chain reaction(PCR),while the histopathology of the lung injury was observed by light microscope.Results Compared with normal group,the expression
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