哮喘大鼠肺组织Akt蛋白表达上调对IL-4,IL-12和IL-13的影响

目的：研究Akt蛋白对支气管哮喘大鼠IL-4,IL-12和IL-13表达的影响。方法：雄性SD大鼠24只,随机分为3组：对照组（C组）、哮喘组（A组）、渥曼宁青霉素组（Wortmannin,W组）,每组8只。以卵白蛋白（OVA）致敏和激发建立大鼠哮喘模型。各组大鼠于末次激发后24h,放血处死。酶联免疫吸附试验（ELISA）测定BALF中IL-4,IL-13和IL-12的浓度;免疫组化法测定肺组织中p-Akt蛋白的表达;Western blot测定肺组织匀浆中p-Akt蛋白的含量。结果：A组p-Akt蛋白的表达明显高于C组,W组p-Akt蛋白的表达低于A组,但仍高于C组;BALF中IL-4,IL-13的含量A组明显高于C组,W组IL-4,IL-13的含量低于A组,但仍高于C组,BALF中IL-12的含量A组明显低于C组,W组IL-12的含量低于C组,但仍高于A组。结论：哮喘大鼠模型中出现了Akt蛋白的激活,细胞因子失衡可能与Akt蛋白的激活有关。

Effect of up-regulation of protein Akt in lung tissue of asthmatic rat on IL-4,IL-12 and IL-13

Objective： To study the effect of protein Akt in asthma airway inflammation of asthmatic rats on the cytokine IL-4,IL-13 and IL-12. Methods： Twenty-four male adult Sprague-Dawley （SD） rats were randomly divided into the control group（C）,the asthma group （A）and Wortmannin group （W）. The rats’ asthma models were established, in which rats were sensitized with OVA and Al （OH）3, and repeatedly exposed to aerosolized ovalbumin. The rats were sacrificed at 24 hours afer last challege,Meanwhile the concentration of IL-4,IL-13 and IL-12 in BALF were measured with ELISA. The expressions of p-Akt protein were detected with Immuno-histochemistry （IHC）. The level of p-Akt in lung homogenate was measured with Western blot. Results： The expressions of p-Akt protein of lung tissues in the group A were higher than those in group C,and the expressions of p-Akt protein of group W were lower than that of group A, but higher than that of group C. The concentration of IL-4 and IL-13 in BALF of group A were significantly higher than that of group C and those of group W were lower than those of group A but higher than those of group C. The concentration of IL-12 in BALF of group A was significantly lower than that of group C and that of group W was lower than that of group C,but higher than that of group A. Conclusion： The protein Akt is activated in the asthmatic rats model,and the imbalance of cytokine and the airway inflammation in the asthmatic rats model maybe regulated by activation of Akt.