Objective： To investigate whether emodin exerts protective effects on mouse with allergic asthma. Methods： A mouse model of allergic airway inflammation was employed. The C57BL/6 mice sensitized and challenged with ...Objective： To investigate whether emodin exerts protective effects on mouse with allergic asthma. Methods： A mouse model of allergic airway inflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin （OVA） were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid （BALF） was measured. The levels of interleukin （IL）-4, IL-5, IL-13 and eotaxin in BALF and level of immunoglobulin E （IgE） in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4, IL-5, home oxygenase （HO）-I and matrix metalloproteinase-9 （MMP- 9） were determined by real-time quantitative polymerase chain reaction. Results： Emodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4, IL-5, IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally, emodin suppressed IL-4, IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression. Conclusion： Emodin exhibits anti-inflammatory activity in the airway inflammation mouse model, supporting its therapeutic potential for the treatment of allergic bronchial asthma.展开更多
基金Supported by the National Program on Key Basic Research Program Project(973 Program,No.2009CB522704)
文摘Objective： To investigate whether emodin exerts protective effects on mouse with allergic asthma. Methods： A mouse model of allergic airway inflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin （OVA） were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid （BALF） was measured. The levels of interleukin （IL）-4, IL-5, IL-13 and eotaxin in BALF and level of immunoglobulin E （IgE） in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4, IL-5, home oxygenase （HO）-I and matrix metalloproteinase-9 （MMP- 9） were determined by real-time quantitative polymerase chain reaction. Results： Emodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4, IL-5, IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally, emodin suppressed IL-4, IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression. Conclusion： Emodin exhibits anti-inflammatory activity in the airway inflammation mouse model, supporting its therapeutic potential for the treatment of allergic bronchial asthma.
