摘要
Objective： To examine the effect of metanol extract of Petiveria alliacea （PM） on airway inflammation in a murine model of chronic asthma. Methods： Two-month-old male BALB/c mice （n=6-8/group） were sensitized on days 0 and 14 by intraperitoneal injection of 20μg ovalbumin （OVA）. On day 25, the mice received an airway challenge with OVA （3%, w/v, in phosphate buffered saline）. PM was administered orally by oral gavage to mice at doses of 100, 200 and 400 mg/kg body weight once daily from days 18 to 23. Control mice were orally administered phosphate buffered saline （PBS） to induce a model of asthma. At the end of the test, respiratory reactivity was assayed, the total cell number, interleukin-4 （IL-4）, IL-5, IL-13, tumor necrosis factor-alpha （TNF-α） and reactive oxygen species （ROS） in the bronchoalveolar lavage fluid （BALF） were determined and the levels of serum IgE, intercellular cell adhesion molecule 1 （ICAM-1） and eotoxin were measured. In addition, lung tissue was used to qualify the IL-4, IL-5, IL-13, TNF-α and transforming growth factor beta 1 （TGF-β1）. Histologic examination was performed to observe inflammatory cellular infiltration. Results： The administration of PM in comparison with the OVA-only treated group significantly attenuated the infiltration of eosinophUs and other inflammatory cells （P〈0.01）. Airway resistance （RI） in the OVA-only induced group was significantly higher than that of the PBS control group （P〈0.01） when methacholine was added. TNF-α, IgE, TGF-β1 and cytokine levels IL-4, IL-5, IL-β in the BALF decreased compared to control mice （P〈0.01 or P〈0.05）. PM treatment also inhibited the production of chemokines, eotaxin and ICAM-1 in BALF （P〈0.01）, which improved lung function. Histopathological examination revealed that the sensitized treated PM groups had significant lower in inflammatory scores similar to dexamethasone treatments and the untreated group. Conclusion： Administration of PM could inhibit airway inflammation, regulate cytokines, chemokines and enhance pulmonary conditions in allergic murine model of asthma.
Objective： To examine the effect of metanol extract of Petiveria alliacea （PM） on airway inflammation in a murine model of chronic asthma. Methods： Two-month-old male BALB/c mice （n=6-8/group） were sensitized on days 0 and 14 by intraperitoneal injection of 20μg ovalbumin （OVA）. On day 25, the mice received an airway challenge with OVA （3%, w/v, in phosphate buffered saline）. PM was administered orally by oral gavage to mice at doses of 100, 200 and 400 mg/kg body weight once daily from days 18 to 23. Control mice were orally administered phosphate buffered saline （PBS） to induce a model of asthma. At the end of the test, respiratory reactivity was assayed, the total cell number, interleukin-4 （IL-4）, IL-5, IL-13, tumor necrosis factor-alpha （TNF-α） and reactive oxygen species （ROS） in the bronchoalveolar lavage fluid （BALF） were determined and the levels of serum IgE, intercellular cell adhesion molecule 1 （ICAM-1） and eotoxin were measured. In addition, lung tissue was used to qualify the IL-4, IL-5, IL-13, TNF-α and transforming growth factor beta 1 （TGF-β1）. Histologic examination was performed to observe inflammatory cellular infiltration. Results： The administration of PM in comparison with the OVA-only treated group significantly attenuated the infiltration of eosinophUs and other inflammatory cells （P〈0.01）. Airway resistance （RI） in the OVA-only induced group was significantly higher than that of the PBS control group （P〈0.01） when methacholine was added. TNF-α, IgE, TGF-β1 and cytokine levels IL-4, IL-5, IL-β in the BALF decreased compared to control mice （P〈0.01 or P〈0.05）. PM treatment also inhibited the production of chemokines, eotaxin and ICAM-1 in BALF （P〈0.01）, which improved lung function. Histopathological examination revealed that the sensitized treated PM groups had significant lower in inflammatory scores similar to dexamethasone treatments and the untreated group. Conclusion： Administration of PM could inhibit airway inflammation, regulate cytokines, chemokines and enhance pulmonary conditions in allergic murine model of asthma.
