基础医学与临床 ›› 2011, Vol. 31 ›› Issue (3): 281-285.

• 研究论文 • 上一篇    下一篇

氯沙坦抑制急性肺损伤大鼠肺组织LOX-1表达

韩鹏凯1,张婷2,王导新3   

  1. 1. 重庆医科大学附属第二医院呼吸内科
    2. 重庆医科大学第二附属医院呼吸内科
    3. 重庆医科大学附属第二医院
  • 收稿日期:2010-07-05 修回日期:2010-08-01 出版日期:2011-03-05 发布日期:2011-03-14
  • 通讯作者: 张婷 E-mail:zhangtng@tom.com
  • 基金资助:
    省卫生厅科研基金

Losartan suppress expression of lectin-like oxidized LDL receptor-1 in lung tissue of ALI rat

  • Received:2010-07-05 Revised:2010-08-01 Online:2011-03-05 Published:2011-03-14
  • Contact: Ting ZHANG E-mail:zhangtng@tom.com

摘要: 目的 研究氯沙坦干预大鼠急性肺损伤模型肺组织血凝素样氧化低密度血浆脂蛋白受体-1(LOX-1)表达的变化,探讨LOX-1在急性肺损伤中的表现及氯沙坦的干预机制。方法 将大鼠随机分成:对照组、脂多糖(LPS)组(5mg/kg)及氯沙坦治疗组(8mg/kg),每组10只。检测动脉血氧分压(PaO2)、肺湿/干质量值(W/D)、支气管肺泡灌洗液(BALF)蛋白含量、血浆和BALF中TNF-α水平及肺组织病理变化,比色法测定肺组织髓过氧化物酶(MPO)活性,用RT-PCR法检测肺组织LOX-1 mRNA水平,western blot法检测肺组织中LOX-1、ICAM-1、Cleaved caspase-3蛋白的表达。结果 脂多糖处理后大鼠肺部炎症反应显著,PaO2较对照组下降,而肺W/D值、BALF蛋白含量及TNF-α水平、血浆TNF-α水平、MPO活性升高(P<0.05);LOX-1 mRNA和LOX-1、ICAM-1及Cleaved caspase-3蛋白表达升高(P<0.05)。氯沙坦显著缓解上述变化(P<0.05)。结论 氯沙坦可能通过抑制LOX-1介导的炎症及细胞凋亡减轻急性肺损伤。

关键词: 急性肺损伤, 氯沙坦, 血凝素样氧化低密度血浆脂蛋白受体-1

Abstract: Objective To study the effect of losartan on expression of lectin-like oxidized LDL receptor-1 (LOX-1) protein in acute lung injury (ALI), to investigate its role in the process and mechanism of the effect of losartan on ALI. Methods Rats were randomly divided into normal control group, lipopolysaccharide (LPS) group (5mg/kg), and LPS+Losartan group, each group 10 rats. Rats in LPS+Losartan group were given an intraperitoneal injection of losartann (8mg/kg) after LPS administration. The level of PaO2, wet/dry ratio(W/D), the concentration of protein and TNF-α in bronchoalveolar lavage fluid (BALF), T?N?F-α concentration in plasma, lung MPO (myeloperoxidase) activity by chromometry and lung tissue histopathological changes were examined, LOX-1 mRNA was detected by RT-PCR analysis, the expression of LOX-1, ICAM-1, Cleaved caspase-3 protein in lung was measured by Western blot. Results Histological examination showed that extensive lung inflammation were seen in the LPS group. The level of PaO2 in LPS group decreased compared with taht in sham group (P<0.05). The level of W/D , concentration of protein in BALF, TNF-α in BALF and plasma, lung MPO activity, the expression of LOX-1 mRNA, LOX-1, ICAM-1 and Cleaved caspase-3 protein in LPS group were increased significantly respectively compared with those in sham group (P<0.05). Compared with LPS group these changes were markedly attenuated in LPS+Losartan group (P<0.05). Conclusion There is protective effect of losartan on ALI, which may result from inhibiting the inflammation and apoptosis induced by LOX-1.

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