哮喘联盟

   摘要
   哮喘是一种复杂的、发病率高的气道疾病，是当前主要的公共健康问题，目前尚无特效治疗方法。目前发现法呢醇X受体(FXR)能在各种疾病状态下产生抗炎作用，但尚无鹅去氧胆酸 (CDCA)，一种天然的FXR激动剂，用于过敏性气道炎症治疗的研究报道。我们建立乳清蛋白（OVA）引起急性哮喘的小鼠模型以测试CDCA在气道炎症中的有效性。通过评估疾病相关的病理学和分子学标记，研究发现，肺组织表达FXR和CDCA给药降低小鼠过敏性气道疾病的严重程度。CDCA治疗使得细胞较少向周围及支气管周围空间浸润，减少杯状细胞肥大、粘液分泌，并降低由乳清蛋白引起的过敏性哮喘小鼠升高的血清IgE水平。CDCA治疗进一步阻滞TH2细胞因子（IL-4, IL-5 and IL-13）的分泌，促炎细胞因子TNF-α提示FXR及其激动剂对于过敏性哮喘具有潜在治疗作用。

 

（杨冬 审校）
BiochemBiophysResCommun. 2015Jun8.pii:S0006-291X(15)30030-9.doi:10.1016/j.bbrc.2015.05.104. [Epub ahead of print]


 

Chenodeoxycholic acid attenuates ovalbumin-induced airway inflammation in murine model of asthma by inhibiting the TH2 cytokines.
 

Shaik FB1, Panati K2, Narasimha VR1, Ramireddy Narala V3.
 

Abstract
Asthma is a complex highly prevalent airway disease that is a major public health problem for which current treatment options are inadequate. Recently, farnesoid X receptor (FXR) have been shown to exert anti-inflammatory actions in various disease conditions, but there have been no reported investigations of Chenodeoxycholic acid (CDCA), a natural FXR agonist, in allergic airway inflammation. To test the CDCA effectiveness in airway inflammation, ovalbumin (OVA)-induced acute murine asthma model was established. We found that lung tissue express FXR and CDCA administration reduced the severity of the murine allergic airway disease as assessed by pathological and molecular markers associated with the disease. CDCA treatment resulted in fewer infiltrations of cells into the airspace and peribronchial areas, and decreased goblet cell hyperplasia, mucus secretion and serum IgE levels which is increased in mice with OVA-induced allergicasthma. The CDCA treatment further blocked the secretion of TH2 cytokines (IL-4, IL-5 and IL-13) and proinflammatory cytokine TNF-α indicate that the FXR and its agonists may have potential for treating allergicasthma.
 

BiochemBiophysResCommun. 2015Jun8.pii:S0006-291X(15)30030-9.doi:10.1016/j.bbrc.2015.05.104. [Epub ahead of print]