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Sini decoction alleviates E. coli induced acute lung injury in mice via equilibrating ACE-AngII-AT1R and ACE2-Ang-(1-7)-Mas axis

机译:Sini汤剂通过平衡ACE-Angii-AT1R和ACE2-Ang-(1-7)-MAS轴通过平衡αce-Ang-(1-7)轴来减轻大肠杆菌诱导小鼠急性肺损伤

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摘要

AimsAcute respiratory distress syndrome (ARDS), one of the serious form of acute lung injury (ALI), is the primary cause of death in patients with ALI. Sini decoction (SND) is a widely used Traditional Chinese Medicine (TCM). However, the application of SND in ALI is rarely reported.Previous studies have found that renin-angiotensin-aldosterone system (RAAS) played vital and bidirectional roles in ALI. Therefore, the aim of the present study was to investigate protective effect of SND on ALI model induced byE. coli, as well as to further explore relations between RAAS and SND. Materials and methodsThe ALI model was evaluated by morphological observations and biochemical assays. The expression levels of angiotensin converting enzyme (ACE), Angiotensin II type 1 receptor (AT1R) and angiotensin converting enzyme 2 (ACE2) were examined by Western blotting. The expression levels of angiotensinII (AngII) and angiotensin-(1-7) (Ang-(1-7)) were measured through ELISA. MasR, IL-6, IL-1β and TNFα were all measured using qRT-PCR. Key findingsSND significantly amelioratedE. coli-induced ALI, including reducing inflammatory factors in lung tissue and the activity of MPO in serum. Furthermore, SND could obviously decrease the expression of ACE, AngII and AT1R, which were induced byE. coli. On the other hand, SND could markedly activate ACE2-Ang-(1-7)-Mas pathway. SignificanceIn this paper, we demonstrated that SND alleviatesE. coliinduced acute lung injury in mice via equilibrating ACE-AngII-AT1R and ACE2-Ang-(1-7)-Mas axis.
机译:Aimsacutute呼吸窘迫综合征(ARDS)是急性肺损伤(ALI)的严重形式之一,是ALI患者死亡的主要原因。 Sini汤(SND)是一种广泛使用的中药(TCM)。然而,SND在ALI中的应用很少报道。另一种研究发现,肾素 - 血管紧张素 - 醛固酮系统(RAAS)在ALI中发挥了重要和双向作用。因此,本研究的目的是研究SND对BYE诱导ALI模型的保护作用。 Coli,以及进一步探索RAA和SND之间的关系。材料和方法通过形态学观察和生物化学测定评估ALI模型。通过蛋白质印迹检查血管紧张素转化酶(ACE),血管紧张素II型受体(AT1R)和血管紧张素转换酶2(ACE2)的表达水平。通过ELISA测量血管紧张素(Angii)和血管紧张素(1-7)(Ang-(1-7))的表达水平。所有使用QRT-PCR测量MasR,IL-6,IL-1β和TNFα。主要发现有显着的疗法。大肠杆菌诱导的Ali,包括减少肺组织中的炎症因子以及血清中MPO的活性。此外,SND可显然可以降低αCE,Angii和AT1R的表达,其诱导再见。大肠杆菌。另一方面,SND可以显着激活ACE2-ANG-(1-7)-MAS途径。这篇论文的意义,我们证明了SND Alleviatese。通过平衡Ace-Angii-AT1R和ACE2-Ang-(1-7)-MAS轴的小鼠急性肺损伤。

著录项

  • 来源
    《Life sciences》 |2018年第2018期|共10页
  • 作者单位

    School of Life Sciences and Technology China Pharmaceutical University;

    Intensive Care Unit Affiliated Hospital of Nanjing University of Traditional Chinese Medicine;

    School of Life Sciences and Technology China Pharmaceutical University;

    School of Life Sciences and Technology China Pharmaceutical University;

    School of Life Sciences and Technology China Pharmaceutical University;

    School of Life Sciences and Technology China Pharmaceutical University;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;
  • 关键词

    Acute lung injury (ALI); Sini decoction (SND); RAAS; ACE; ACE2;

    机译:急性肺损伤(ALI);SINI汤(SND);RAAS;ACE;ACE2;

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