| 冯英同 高春城 叶福林 朱建福 冯英备 王增辉 周峰 黄兵.褪黑素通过激活SIRT1 信号通路发挥抗肺缺血再灌注损伤作用[J].,2017,17(2):242-246 |
| 褪黑素通过激活SIRT1 信号通路发挥抗肺缺血再灌注损伤作用 |
| Melatonin Exerts Protective Effect on Lung Ischemia Reperfusion Injury byActivating the SIRT1 Signaling Pathway |
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| DOI： |
| 中文关键词: 肺缺血再灌注损伤 褪黑素 沉默信息调控因子1 |
| 英文关键词: Lung ischemia reperfusion injury Melatonin SIRT1 |
| 基金项目:国家自然科学基金项目（81201583）；南京军区创新课题（15MS043） |
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| 中文摘要: |
| 目的：研究褪黑素（Melatonin，Mel）在肺缺血再灌注损伤中的作用，明确沉默信息调控因子1（Silent information regulator 1，
SIRT1）信号通路在这一过程中的关键作用。方法：建立大鼠肺缺血再灌注损伤（IR）模型，实验分为Control、IR、IR+10 mg/Kg Mel、
IR+20 mg/Kg Mel、IR+30 mg/Kg Mel 五组，通过检测支气管肺泡灌洗液中白细胞数目、蛋白含量和肺组织中丙二醛（MDA）水平、
干湿重比等指标明确肺组织损伤程度，Western blot检测SIRT1 通路相关分子及凋亡相关蛋白的表达水平，研究其作用机制。结
果：与IR 组相比，Mel 处理显著降低了支气管肺泡灌洗液中白细胞数量、蛋白含量和肺组织MDA 含量、干湿重比（P<0.05）；Mel
还显著上调了SIRT1 表达，降低了Ac-FOXO1表达（P<0.05）；此外，Mel 显著提高了抗凋亡蛋白Bcl-2 表达，下调了凋亡蛋白Bax
表达（P<0.05）。结论：Mel 具有明确的抗肺缺血再灌注损伤的作用，SIRT1 信号通路在该过程中可能扮演重要角色。 |
| 英文摘要: |
| Objective:To investigate the protective effect of melatonin (Mel) on lung ischemia reperfusion injury as well as
SIRT1's role in this process.Methods:The rat lung ischemia reperfusion injury model was established to mimic the clinical lung ischemia
reperfusion injury (IRI). The rats were divided into Control group, IR, IR+10 mg/Kg Mel, IR+20 mg/Kg Mel, IR+30 mg/Kg Mel group.
The white blood cells and protein in bronchoalveolar lavage fluid, malondialdehyde in lung tissue and the wet/dry ratio of lung tissue
were detected. In addition, the SIRT1, Ac-FOXO1, Bcl-2, and Bax expression were detected by Western blot.Results:Compared with
the IR group, Mel treatment significantly reduced the number of white blood cells and the content of protein in bronchoalveolar lavage
fluid, the level of malondialdehyde in lung tissue and the wet/dry ratio of lung tissue (P<0.05). Mel also significantly increased Bcl2
expression and decreased Bax expression (P<0.05). In addition, the SIRT1 expression was up-regulated compared with the IR group and
Ac-FOXO1 expression was down-regulated compared with the IR group (P<0.05).Conclusion:Mel can significantly alleviate lung IRI,
which might be mediated via SIRT1 activation. |
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