RESUMO
Objective To investigate the effect and mechanism of compound glycyrrhizin on airway inflammation in asthmatic rats. Methods Forty wistar rats were randomly divided into health group (group Ⅰ), asthma group(group Ⅱ), treating group (group Ⅲ) and treating control group (group Ⅳ) (n=10 in each group). Group Ⅱ, group Ⅲ and group Ⅳ received intraperitoneal injection of ovalbumin (OVA) and aluminum hydroxide gel for sensitization and OVA aerosol by ultrasonic nebulization for challenge, in addition, group Ⅲ re-ceived intraperioneal injection of 200 μg of compound glycyrrhizin 1 hour before OVA aerosol challenging every time, and group Ⅳ were in-jected with normal saline instead of compound glycyrrhizin. Group Ⅰ were injected and nebulizated with normal saline instead of OVA and alu-minlum hydroxide. All rats were sacrificed at the 6th hour after the last challenging, venous blood and bronchoalveolar lavage fluid(BALF) were collected, the IgE in venous blood were determined and the concentration of IL-4, IL-5, IL-13 and IFN-γ in BALF were detected, the cells in BALF were counted and detached. Results The concentration of IgE, IL-4, IL-5, IL-13 and the count of neutrophilic granulocytcs, lymphocytes, cosinophils in group Ⅱ were significantly higher than those in group Ⅰ and group Ⅲ(P<0.01), and the concentration of IFN-γ in group Ⅰ and group Ⅳ were significantly lower than those in group Ⅰ and group Ⅲ(P <0.01). There was no significant difference be-tween group Ⅱ and group Ⅳ(P >0. 05). The concentration of IgE, IL-4, IL-5, IL-13 and the count of neutrophilic granulocytes, lympho-cytes, cosinophils in group Ⅲ were higher than those in group Ⅰ, and the concentration of IFN-γ and the count of mononucleat macroplile cells in group Ⅲ were lower than those in group Ⅰ, but there were no significant difference(P>0.05). Conclusion Compound giycyrrhiz-in alleviated the airway inflammation and reduced the airway hyperresponsiveness in asthmatic rats, which mechanism may be related to regu-lating the balance of Th1/Th2 cytokines, suppressing the immune ability of Th2 and promoting the immune ability of Th1.