کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2548032 | 1124078 | 2007 | 8 صفحه PDF | دانلود رایگان |

Eosinophils have been implicated in a broad range of diseases, most notably allergic conditions (e.g. asthma, rhinitis and atopic dermatitis) and inflammatory diseases. These diseases are characterized by an accumulation of eosinophils in the tissue. Defining the mechanisms that control eosinophil recruitment is fundamental to understanding how these diseases progress and may identify a novel target for drug therapy. Eotaxin is a potent eosinophil-specific chemokine that is released in the respiratory epithelium after allergic stimulation.Aim of the studyIn this study, we determined whether Moutan Cortex Radicis (MCR), a plant extract, effects eotaxin secretion from A549 epithelial cells and eosinophil chemotaxis, and then examined the mechanism involved.Materials and methodsPrior to assaying MCR's effects, A549 cells were stimulated with tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4) and IL-1β to induce expression of chemokines and adhesion molecules involved in eosinophil chemotaxis. In the presence of MCR, eotaxin, regulated on activation in normal T cells expressed and secreted (RANTES), IL-8, IL-16, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) transcripts were quantitated by real-time RT-PCR.ResultsAs a result, 0.01, 1, and 100 μg/ml of MCR treatments reduced eotaxin expression significantly and 0.01, 0.1, 1, 10, and 100 μg/ml of MCR reduced significantly eotaxin secretion. In addition, MCR treatment significantly inhibited eosinophil migration toward A549 medium. And 100 μg/ml of MCR suppressed the activated of nuclear factor (NF)-κB.ConclusionsThese findings indicate that suppressed eotaxin secretion by MCR treatment is due to the inhibition of NF-κB activation. Therefore, MCR might be of therapeutic value in treating asthma.
Journal: Journal of Ethnopharmacology - Volume 114, Issue 2, 1 November 2007, Pages 186–193