摘要
目的:研究黄芩苷调节哮喘模型小鼠Th1/Th2反应的分子机制。方法:将BALB/c小鼠随机分为6组,分别为正常对照组、模型组、地塞米松阳性对照组及黄芩苷高、中、低剂量组。采用卵蛋白(OVA)腹腔注射致敏与雾化吸入激发法复制哮喘模型,末次激发24 h后处死小鼠,取脾,制备单核细胞悬液,以OVA刺激,培养3 d后取培养上清,应用ELISA法检测其中干扰素γ(IFN-γ)、白细胞介素4(IL-4)、白细胞介素5(IL-5)及白细胞介素10(IL-10)的含量;脾细胞培养2 d后用逆转录PCR(RT-PCR)检测T-bet、GATA-3及STAT-6的表达。结果:黄芩苷能显著抑制IL-4、IL-5的蛋白表达及GATA-3、STAT-6的基因表达;并能提高IL-10的蛋白表达。结论:黄芩苷在体内可能主要通过GATA-3、信号转导和转录激活因子6(STAT-6)等转录因子及IL-10调节Th2反应。
Objective ： To study the mechanism of baicalin on the cytokines of Thl/Th2 in rnurine model of asthma. Methods ： The murine model of asthma was induced by OVA. Different doses of baicalin were orally administered to the mice respectively. The spleen cells were cultured 3 days for the measurement of IFN-γ, IL4, IL-5 and IL-10 by ELISA. After 2 days of culture, the spleen cells were treated with Trizol for extraction of total RNA. The gene expressions of T-bet, GATA-3 and STAT-6 were analyzed by RT-PCR. Resuits ：The treatment with baicalin obviously decreased the production of IL4 and IL-5 and the gene expression of GATA-3 ,STAT-6 ,but increased the production of IL-10. Conclusion：Baicalin may modulate the Th1/Th2 balance mainly by alterating the gene expressions of GATA-3 and STAT-6 in vivo and increasing the production of IL-10.
出处
《中药材》
CAS
CSCD
北大核心
2009年第9期1407-1410,共4页
Journal of Chinese Medicinal Materials
基金
2007年暨南大学青年基金(51208022)
广东省中医药局建设中医药强省科研课题(2008096)
