کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5834088 | 1122640 | 2011 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Modulatory effect of anisodamine on airway hyper-reactivity and eosinophilic inflammation in a murine model of allergic asthma
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
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چکیده انگلیسی
Anisodamine, a peripheral muscarinic receptor antagonist, is a naturally occurring atropine derivative that has been isolated, synthesized and characterized by scientists in China. In the present investigation, we evaluated the modulatory effects of anisodamine on airway hyper-reactivity and inflammation in a murine model of allergic asthma. Asthma model was induced successfully by ovalbumin. The activation of cells, airway eosinopilia, cytokine production, and airway function were examined. Our results collectively show that anisomanine could significantly suppress the accumulation of eosinophils into the airways and dramatically inhibited the histological changes in OVA-induced mice. Additionally, anisodamine could restore the Th1/Th2 balance in BALF by downregulating the level of Th2 cell-associated cytokine IL-4 (p < 0.01) and upregulating the level of Th1 cell-associated cytokine IFN-γ (p < 0.01). In addition, pretreatment with anisodamine also showed strong suppression of allergen-induced bronchial hyper-reactivity with maximum contraction decreasing from 0.45 ± 0.02 g to 0.28 ± 0.03 g (p < 0.01). These results suggested the modulatory effects of anisodamine on Th1/Th2 balance by enhancing Th1-related and suppressing Th2-related parameters, as well as its potential application in airway hyper-reactivity and eosinophilic inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 11, Issue 2, February 2011, Pages 260-265
Journal: International Immunopharmacology - Volume 11, Issue 2, February 2011, Pages 260-265
نویسندگان
Zu-Peng Xu, Hao Wang, Li-Na Hou, Zheng Xia, Liang Zhu, Hong-Zhuan Chen, Yong-Yao Cui,