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祝 卿, 周文琴, 万 里, 等.1-磷酸鞘氨醇及受体1在小鼠肺缺血再灌注损伤中的表达变化和意义.四川大学学报(医学版),2018,49(6):891-894
1-磷酸鞘氨醇及受体1在小鼠肺缺血再灌注损伤中的表达变化和意义
The Expression of Sphingosine-1-phosphate and Sphingosine-1-phosphate Receptor 1 in Mouse Model of Pulmonary Ischemia-Reperfusion Injury
  
中文关键词:  1-磷酸鞘氨醇 1-磷酸鞘氨醇受体1 肺缺血再灌注
英文关键词:S1P S1PR Pulmonary ischemia reperfusion
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中文摘要:
      目的 探讨1-磷酸鞘氨醇(sphingosine-1-phosphate,S1P)及其受体1(S1PR1)在肺缺血再灌注损伤(PIRI)肺组织中的表达变化及意义。方法 采用无损伤血管夹阻断小鼠左主支气管、左肺静脉和左肺动脉缺血30 min,松开血管夹,接受再灌注2 h,制作小鼠PIRI模型(n=8),同时设正常对照组(n=8)和假手术组(n=8),3组小鼠均处死后取肺组织。根据肺组织HE染色、湿/干质量比结果论证模型制作情况。采用实时荧光定量聚合酶链反应检测肺组织中生成S1P的关键限速酶鞘氨醇激酶-1(SphK1)S1PR1 mRNA表达变化;酶联免疫吸附法(ELISA) 检测肺组织中S1P及S1PR1蛋白含量的变化。结果 与正常对照组和假手术组比较,缺血再灌注可导致肺组织病理评分升高,肺干/湿质量比增高,肺组织SphK1和S1PR1 mRNA表达升高(P<0.05),肺组织中S1P、S1PR1蛋白含量均明显增加(P<0.05)。结论 PIRI后,肺组织中S1P及S1PR1的表达升高,提示S1P/S1PR1信号通路参与了PIRI的病理生理改变过程,可能是PIRI潜在的治疗靶点。
英文摘要:
      Objective To investigate the expressions of sphingosine 1-phosphate (S1P) and S1P G-protein-coupled receptor 1 (S1PR1) in pulmonary ischemia reperfusion injury (PIRI) tissues and explore their relationship.Methods The model of PIRI was established in vivo male C57BL/6 mice (n=8). The left pulmonary hilum was occluded for 30 min with a microvascular clamp through a left thoracotomy. Reperfusion began with removal of the clamp. Normal group (n=8) and sham group (n=8) were set as control. The hematoxylin and eosin (HE) staining of ultrastructural changes and wet-to-dry mass ratio in lung tissues were measured for judging the succeed model. The mRNA expressions of sphingosine kinase 1 (SphK1) and S1PR1 were determined by real-time PCR, and ELISA was used to detect the concentrations of S1P and S1PR1 in the lung tissues. Results The mRNA expressions of SphK1, S1PR1 and the concentrations of S1P and S1PR1 and wet-to-dry mass ratio of the lung tissues in ischemia-reperfusion mice were higher than those normal mice and sham operation mice (P<0.05). Conclusion The increased expressions of S1P and S1PR1 in lung tissues after PIRI suggest that the S1P/S1PR1 signal pathway is involved in the pathophysiological process of PIRI, and may be a potential therapeutic target for it.
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