文章摘要
纪木火1 吴晶1 田蜜1 李仁奇1 李国民2 范云霞2 杨建军1△.HMGB1 在a2A- 肾上腺素受体介导脓毒血症大鼠急性肺损伤的作用[J].,2012,12(2):215-217
HMGB1 在a2A- 肾上腺素受体介导脓毒血症大鼠急性肺损伤的作用
Effect of High Mobility Group Box-1 Protein onα2A-Adrenoceptors-Mediated Acute Lung Injury in a Rat Model of Sepsis
  
DOI:
中文关键词: 高迁移率族蛋白-1  a2A- 肾上腺素受体  脓毒症  急性肺损伤
英文关键词: HMGB1  α2A-adrenaline receptors  Sepsis  Acute lung injury
基金项目:江苏省" 六大人才高峰" 课题(2008093);常州市卫生局科技计划项目(WZ201044)
作者单位
纪木火1 吴晶1 田蜜1 李仁奇1 李国民2 范云霞2 杨建军1△ 南京大学医学院南京军区南京总医院麻醉科 
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中文摘要:
      目的:探讨HMGB1 在a2A- 肾上腺素受体介导脓毒血症大鼠急性肺损伤(ALI)的作用。方法:64 大鼠建立盲肠结扎穿孔法 (CLP)脓毒症模型,随机均分为以下两组:CLP 组及CLP+ 马来酸钠组。各组分别于模型建立后2(T1)、6(T2)、12(T3)、24 h(T4)时 检测大鼠血清TNF- 、高迁移率族蛋白1(HMGB1)及IL-10 含量。CLP24 h 后检测肺组织干湿重比(W/D)和髓过氧化物酶活性 (MPO)及HMGB1 表达;并采用HE 法进行肺组织学评分。结果:CLP+ 马来酸钠组T2 时的TNF- 水平明显低于CLP 组(P<0.05); 而HMGB1 在T2、T3 及T4 均明显低于CLP 组(P<0.05);IL-10 在各个时间点比较结果差异无统计学意义(P>0.05)。CLP+ 马来酸 钠组肺组织W/D、MPO 活性、肺组织损伤评分均明显低于CLP 组(P<0.05)。CLP+ 马来酸钠组肺组织HMGB1 表达明显低于CLP 组(P<0.05)。结论:HMGB1 参与了ALI 的病理过程, a2A- 肾上腺素受体阻断可以通过抑制HMGB1 从而改善ALI 时的肺功能。
英文摘要:
      Objective: To investigate the effect of high mobility group box-1 protein on α2A-adrenaline receptors-mediated acute lung injury in a rat model of sepsis. Methods: In a sepsis model by cecal ligation and puncture (CLP), sixty-four SD rats were randomly divided into the following groups: CLP group and CLP + maleate group. Plasma levels of TNF-α, HMGB1 and IL-10 were determined at the following time points: 2 (T1), 6 (T2), 12 (T3) and 24 h (T4) after CLP. Lung was removed for the determinations of pulmonary wet-to-dry ratio (W/D), myeloperoxidase activity (MPO), total histological scores and HMGB1 immunohistochemistry analysis 24 h after CLP. Results: Plasma levels of TNF-α at T2 and HMGB1 at T2, T3 and T4 were significantly lower in CLP + maleate group than CLP group (P<0.05). There was no difference in IL-10 over time between groups (P>0.05). Pulmonary levels of W/D, MPO, total histological scores and HMGB1 expression were significantly lower than those in CLP group (P<0.05). Conclusions: HMGB1 plays a key role in the pathophysiology of ALI, and antagonism of α2A-adrenoceptors improves pulmonary function by inhibiting HMGB1.
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