| 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].现代生物医学进展英文版,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 |
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| 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） |
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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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